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CHAPTER 19
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The Cardiovascular
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System: The Blood

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Blood and Homeostasis

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Blood contributes to homeostasis by transporting oxygen, carbon dioxide, nutrients, and hormones
to and from your body’s cells. It also helps regulate body pH and temperature, and provides
protection against disease through phagocytosis and the production of antibodies.
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The focus of this chapter is blood; the next two chapters will examine its differences through various blood tests when trying to determine the
the heart and blood vessels, respectively. Blood transports various cause of different diseases.
substances, helps regulate several life processes, and affords protection
against disease. For all of its similarities in origin, composition, and Q Did you ever wonder how analyzing blood can determine
functions, blood is as unique from one person to another as are skin, if we are healthy, detect a multitude of infections, and
bone, and hair. Health-care professionals routinely examine and analyze detect or rule out various diseases and injuries?
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19.1 Functions and Properties of Blood 669

injury. In addition, its white blood cells protect against disease by

19.1 Functions and Properties carrying on phagocytosis. Several types of blood proteins, includ-
ing antibodies, interferons, and complement, help protect against
of Blood
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disease in a variety of ways.

OBJECTIVES Physical Characteristics of Blood

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• Explain the functions of blood. Blood is denser and more viscous (thicker) than water and feels
• Describe the physical characteristics and principal components of slightly sticky. The temperature of blood is 38°C (100.4°F), about 1°C
blood. higher than oral or rectal body temperature, and it has a slightly alka-
line pH ranging from 7.35 to 7.45 (average = 7.4). The color of blood
varies with its oxygen content. When saturated with oxygen, it is bright
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The cardiovascular system (cardio- = heart; vascular = blood or red. When unsaturated with oxygen, it is dark red. Blood constitutes
blood vessels) consists of three interrelated components: blood, the about 20% of extracellular fluid, amounting to 8% of the total body
heart, and blood vessels. The branch of science concerned with the mass. The blood volume is 5 to 6 liters (1.5 gal) in an average-sized
study of blood, blood-forming tissues, and the disorders associated adult male and 4 to 5 liters (1.2 gal) in an average-sized adult female.
with them is hematology (hēm-a-TOL-ō-jē; hema- or hemato- =
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The gender difference in volume is due to differences in body size.
blood; -logy = study of). Several hormones, regulated by negative feedback, ensure that blood
Most cells of a multicellular organism cannot move around to ob- volume and osmotic pressure remain relatively constant. Especially
tain oxygen and nutrients or eliminate carbon dioxide and other important are the hormones aldosterone, antidiuretic hormone, and
wastes. Instead, these needs are met by two fluids: blood and intersti- atrial natriuretic peptide, which regulate how much water is excreted
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tial fluid. Blood is a liquid connective tissue that consists of cells sur- in the urine (see Section 27.1).
rounded by a liquid extracellular matrix. The extracellular matrix is
called blood plasma, and it suspends various cells and cell fragments. Clinical Connection
Interstitial fluid is the fluid that bathes body cells (see Figure 27.1)
and is constantly renewed by the blood. Blood transports oxygen Withdrawing Blood
from the lungs and nutrients from the gastrointestinal tract, which
Blood samples for laboratory testing may be obtained in several ways.
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diffuse from the blood into the interstitial fluid and then into body
The most common procedure is venipuncture (vēn′-i-PUNK-chur), with-
cells. Carbon dioxide and other wastes move in the reverse direction, drawal of blood from a vein using a needle and collecting tube, which
from body cells to interstitial fluid to blood. Blood then transports the contains various additives. A tourniquet is wrapped around the arm above
wastes to various organs—the lungs, kidneys, and skin—for elimin- the venipuncture site, which causes blood to accumulate in the vein. This
ation from the body.
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increased blood volume makes the vein stand out. Opening and closing
the fist further causes it to stand out, making the venipuncture more suc-
cessful. A common site for venipuncture is the median cubital vein anterior
Functions of Blood to the elbow (see Figure 21.26c). Another method of withdrawing blood
is through a finger or heel stick. Diabetic patients who monitor their daily
Blood has three general functions: blood sugar typically perform a finger stick, and it is often used for drawing
blood from infants and children. In an arterial stick, blood is withdrawn
y,
1. Transportation. As you just learned, blood transports oxygen from from an artery; this test is used to determine the level of oxygen in oxygen-
the lungs to the cells of the body and carbon dioxide from the body ated blood.
cells to the lungs for exhalation. It carries nutrients from the gastro-
intestinal tract to body cells and hormones from endocrine glands
to other body cells. Blood also transports heat and waste products
to various organs for elimination from the body. Components of Blood
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2. Regulation. Circulating blood helps maintain homeostasis of all Whole blood has two components: (1) blood plasma, a watery liquid
body fluids. Blood helps regulate pH through the use of buffers extracellular matrix that contains dissolved substances, and (2) formed
(chemicals that convert strong acids or bases into weak ones). It elements, which are cells and cell fragments. If a sample of blood is
also helps adjust body temperature through the heat-absorbing centrifuged (spun) in a small glass tube, the cells (which are more
and coolant properties of the water (see Section 2.4) in blood plasma dense) sink to the bottom of the tube while the plasma (which is less
20
and its variable rate of flow through the skin, where excess heat dense) forms a layer on top (Figure 19.1a). Blood is about 45% formed
can be lost from the blood to the environment. In addition, blood elements and 55% blood plasma. Normally, more than 99% of the
osmotic pressure influences the water content of cells, mainly formed elements are cells named for their red color—red blood cells
through interactions of dissolved ions and proteins. (RBCs). Pale, colorless white blood cells (WBCs) and platelets occupy
3. Protection. Blood can clot (become gel-like), which protects less than 1% of the formed elements. Because they are less dense than
against its excessive loss from the cardiovascular system after an red blood cells but more dense than blood plasma, they form a very

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670 CH A PT E R 19 The Cardiovascular System: The Blood

FIGURE 19.1 Components of blood in a normal adult.

Blood is a connective tissue that consists of blood plasma (liquid) plus formed elements (red
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blood cells, white blood cells, and platelets).

Functions of Blood 3. Protects against blood loss

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1. Transports oxygen, carbon through clotting, and against
dioxide, nutrients, hormones, disease through phagocytic Blood plasma (55%)
heat, and wastes. white blood cells and proteins
2. Regulates pH, body temperature, such as antibodies, interferons,
and complement. Buffy coat,
and water content of cells. composed of
white blood cells
Red blood cells
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and platelets
(45%)

(a) Appearance of centrifuged blood

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WHOLE BLOOD BLOOD PLASMA Proteins Albumins 54%
8% 55% 7%
Globulins 38%
Other fluids Fibrinogen 7%
and tissues Water
92% 91.5% All others 1%
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Electrolytes
Nutrients
Gases
Regulatory
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substances
Other solutes Waste products
1.5%

BLOOD PLASMA (weight) SOLUTES

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FORMED ELEMENTS PLATELETS Neutrophils

45% 150,000–400,000 60–70%

WHITE BLOOD CELLS

5000–10,000
y,

RED BLOOD CELLS

Lymphocytes
4.8–5.4 million
20–25%

Monocytes
3–8%
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Eosinophils
2–4%

Basophils
0.5–1.0%
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BODY WEIGHT VOLUME FORMED ELEMENTS WHITE BLOOD CELLS
(number per μ L)
(b) Components of blood

Q What is the approximate volume of blood in your body?

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19.1 Functions and Properties of Blood 671

thin buffy coat layer between the packed RBCs and plasma in centri- Formed Elements The formed elements of the blood include
fuged blood. Figure 19.1b shows the composition of blood plasma three principal components: red blood cells, white blood cells, and
and the numbers of the various types of formed elements in blood. platelets (Figure 19.2). Red blood cells (RBCs) or erythrocytes transport
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oxygen from the lungs to body cells and deliver carbon dioxide from
Blood Plasma When the formed elements are removed from body cells to the lungs. White blood cells (WBCs) or leukocytes protect
blood, a straw-colored liquid called blood plasma (or simply plasma) the body from invading pathogens and other foreign substances.
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is left. Blood plasma is about 91.5% water and 8.5% solutes, most There are several types of WBCs: neutrophils, basophils, eosinophils,
of which (7% by weight) are proteins. Some of the proteins in blood monocytes, and lymphocytes. Lymphocytes are further subdivided into
plasma are also found elsewhere in the body, but those confined to B lymphocytes (B cells), T lymphocytes (T cells), and natural killer (NK)
blood are called plasma proteins. Hepatocytes (liver cells) synthesize cells. Each type of WBC contributes in its own way to the body’s defense
-
most of the plasma proteins, which include the albumins (al′-BU- mechanisms. Platelets, the final type of formed element, are fragments
mins) (54% of plasma proteins), globulins (GLOB-ū-lins) (38%), and of cells that do not have a nucleus. Among other actions, they release
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fibrinogen (fī-BRIN-ō-jen) (7%). Certain blood cells develop into cells chemicals that promote blood clotting when blood vessels are damaged.
that produce gamma globulins, an important type of globulin. These Platelets are the functional equivalent of thrombocytes, nucleated cells
plasma proteins are also called antibodies or immunoglobulins (im′- found in lower vertebrates that prevent blood loss by clotting blood.
ū-nō-GLOB-ū-lins) because they are produced during certain immune The percentage of total blood volume occupied by RBCs is called
responses. Foreign substances (antigens) such as bacteria and viruses the hematocrit (hē-MAT-ō-krit); a hematocrit of 40 indicates that 40%
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stimulate production of millions of different antibodies. An antibody of the volume of blood is composed of RBCs. The normal range of he-
binds specifically to the antigen that stimulated its production and matocrit for adult females is 38–46% (average = 42); for adult males, it
thus disables the invading antigen. is 40–54% (average = 47). The hormone testosterone, present in much
Besides proteins, other solutes in plasma include electrolytes, higher concentration in males than in females, stimulates synthesis of
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nutrients, regulatory substances such as enzymes and hormones, erythropoietin (EPO), the hormone that in turn stimulates production
gases, and waste products such as urea, uric acid, creatinine, am- of RBCs. Thus, testosterone contributes to higher hematocrits in males.
monia, and bilirubin. Lower values in women during their reproductive years also may be
Table 19.1 describes the chemical composition of blood plasma. due to excessive loss of blood during menstruation. A significant drop in

TA B LE 1 9 . 1
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Substances in Blood Plasma

CONSTITUENT DESCRIPTION FUNCTION

Water (91.5%) Liquid portion of blood. Solvent and suspending medium. Absorbs, transports, and
releases heat.
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Plasma proteins (7%) Most produced by liver. Responsible for colloid osmotic pressure. Major contributors to
blood viscosity. Transport hormones (steroid), fatty acids, and
calcium. Help regulate blood pH.
Albumins Smallest and most numerous plasma proteins. Help maintain osmotic pressure, an important factor in the
exchange of fluids across blood capillary walls.
Globulins Large proteins (plasma cells produce Immunoglobulins help attack viruses and bacteria. Alpha and
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immunoglobulins). beta globulins transport iron, lipids, and fat-soluble vitamins.
Fibrinogen Large protein. Plays essential role in blood clotting.
Other solutes (1.5%)
Electrolytes Inorganic salts; positively charged (cations) Na+, Help maintain osmotic pressure and play essential roles in cell
K+, Ca2+, Mg2+; negatively charged (anions) Cl−, functions.
HPO42−, SO42−, HCO3−.
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Nutrients Products of digestion, such as amino acids, glucose, Essential roles in cell functions, growth, and development.
fatty acids, glycerol, vitamins, and minerals.
Gases Oxygen (O2). Important in many cellular functions.
Carbon dioxide (CO2). Involved in the regulation of blood pH.
Nitrogen (N2). No known function.
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Regulatory substances Enzymes. Catalyze chemical reactions.
Hormones. Regulate metabolism, growth, and development.
Vitamins. Cofactors for enzymatic reactions.
Waste products Urea, uric acid, creatine, creatinine, bilirubin, Most are breakdown products of protein metabolism that are
ammonia. carried by the blood to organs of excretion.

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672 CH A PT E R 19 The Cardiovascular System: The Blood

FIGURE 19.2 Formed elements of blood.

The formed elements of blood are red blood cells (RBCs), white blood cells (WBCs), and platelets.
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White blood cell

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(leukocyte: neutrophil)

Blood plasma

Red blood cell

White blood cell (erythrocyte)
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Platelet
Platelet

Red blood cell

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White blood cell
(leukocyte: monocyte)

Juergen Berger/Science Source Images SEM 3500x Mark Nielsen LM 400x

(a) Scanning electron micrograph (b) Blood smear (thin film of blood spread on a glass slide)
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Q Which formed elements of the blood are cell fragments?

hematocrit indicates anemia, a lower-than-normal number of RBCs. In Although some lymphocytes have a lifetime measured in years, most
polycythemia (pol′-ē-sī-THĒ-mē-a) the percentage of RBCs is abnor- formed elements of the blood last only hours, days, or weeks, and
mally high, and the hematocrit may be 65% or higher. This raises the must be replaced continually. Negative feedback systems regulate
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viscosity of blood, which increases the resistance to flow and makes the the total number of RBCs and platelets in circulation, and their
blood more difficult for the heart to pump. Increased viscosity also con- numbers normally remain steady. The abundance of the different
tributes to high blood pressure and increased risk of stroke. Causes of types of WBCs, however, varies in response to challenges by invading
polycythemia include abnormal increases in RBC production, tissue pathogens and other foreign antigens.
hypoxia, dehydration, blood doping, or the use of EPO by athletes. The process by which the formed elements of blood develop is
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called hemopoiesis (hēm-ō-poy-Ē-sis; -poiesis = making) or hemato-
Checkpoint poiesis. Before birth, hemopoiesis first occurs in the yolk sac of an em-
bryo and later in the liver, spleen, thymus, and lymph nodes of a fetus.
1. In what ways is blood plasma similar to interstitial fluid? How
Red bone marrow becomes the primary site of hemopoiesis in the last
does it differ?
3 months before birth, and continues as the source of blood cells after
2. What substances does blood transport?
y,
birth and throughout life.
3. How many kilograms or pounds of blood are there in your body? Red bone marrow is a highly vascularized connective tissue lo-
4. How does the volume of blood plasma in your body compare to cated in the microscopic spaces between trabeculae of spongy bone
the volume of fluid in a 2-liter bottle of Coke? tissue. It is present chiefly in bones of the axial skeleton, pectoral and
pelvic girdles, and the proximal epiphyses of the humerus and femur.
5. List the formed elements in blood plasma and describe their
functions.
About 0.05–0.1% of red bone marrow cells are called pluripotent
20
stem cells (ploo-RI-pō-tent; pluri- = several) or hemocytoblasts and
6. What is the significance of lower-than-normal or higher-than-
are derived from mesenchyme (tissue from which almost all connec-
normal hematocrit?
tive tissues develop). These cells have the capacity to develop into
many different types of cells (Figure 19.3). In newborns, all bone mar-
row is red and thus active in blood cell production. As an individual
19.2 Formation of Blood Cells ages, the rate of blood cell formation decreases; red bone marrow in
20
the medullary (marrow) cavity of long bones becomes inactive and is
replaced by yellow bone marrow, which consists largely of fat cells.
OBJECTIVE Under certain conditions, such as severe bleeding, yellow bone mar-
row can revert to red bone marrow; this occurs as blood-forming stem
• Explain the origin of blood cells. cells from red bone marrow move into yellow bone marrow, which is
then repopulated by pluripotent stem cells.

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19.2 Formation of Blood Cells 673

FIGURE 19.3 Origin, development, and structure of blood cells. A few of the generations of some
cell lines have been omitted.
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Blood cell production, called hemopoiesis, occurs mainly in red bone marrow after birth.

Key:
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Key:
Progenitor cells
CFU–E Colony-forming unit—erythrocyte
Precursor cells or "blasts"
CFU–Meg Colony-forming unit—megakaryocyte
Formed elements of circulating blood Pluripotent stem cell CFU–GM Colony-forming unit—granulocyte
macrophage
Tissue cells
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Myeloid stem cell

Lymphoid stem cell

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CFU–E CFU–Meg CFU–GM

Proerythroblast Megakaryoblast Eosinophilic Basophilic Myeloblast Monoblast T lymphoblast B lymphoblast NK lymphoblast

myeloblast myeloblast
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Nucleus
ejected

Reticulocyte Megakaryocyte
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Red blood cell Platelets Eosinophil Basophil Neutrophil Monocyte T lymphocyte B lymphocyte Natural
(erythrocyte) (T cell) (B cell) killer (NK) cell

Granular leukocytes Agranular leukocytes

y,

Mast cell Macrophage Plasma cell

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Q From which connective tissue cells do pluripotent stem cells develop?

Stem cells in red bone marrow reproduce themselves, prolifer- marrow cells. Blood from nutrient and metaphyseal arteries (see
20
ate, and differentiate into cells that give rise to blood cells, mac- Figure 6.4) enters a bone and passes into the enlarged and leaky
rophages, reticular cells, mast cells, and adipocytes. Some stem cells capillaries, called sinuses, that surround red bone marrow cells and
can also form osteoblasts, chondroblasts, and muscle cells, and may fibers. After blood cells form, they enter the sinuses and other blood
be destined for use as a source of bone, cartilage, and muscular tissue vessels and leave the bone through nutrient and periosteal veins (see
for tissue and organ replacement. The reticular cells produce reticular Figure 6.4). With the exception of lymphocytes, formed elements do
fibers, which form the stroma (framework) that supports red bone not divide once they leave red bone marrow.

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674 CH A PT E R 19 The Cardiovascular System: The Blood

leads to a decreased ability to deliver oxygen to body tissues. Throm-

Clinical Connection
bopoietin (TPO) (throm′-bō-POY-ē-tin) is a hormone produced by the
liver that stimulates the formation of platelets from megakaryocytes.
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Bone Marrow Examination Several different cytokines regulate development of different blood
Sometimes a sample of red bone marrow must be obtained in order to diag-
-
cell types. Cytokines (SI -tō-kīns) are small glycoproteins that are typ-
nose certain blood disorders, such as leukemia and severe anemias. Bone ically produced by cells such as red bone marrow cells, leukocytes,
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marrow examination may involve bone marrow aspiration (withdrawal of a macrophages, fibroblasts, and endothelial cells. They generally act as
small amount of red bone marrow with a fine needle and syringe) or a bone local hormones (autocrines or paracrines; see Chapter 18). Cytokines
marrow biopsy (removal of a core of red bone marrow with a larger needle).
stimulate proliferation of progenitor cells in red bone marrow and
Both types of samples are usually taken from the iliac crest of the hip regulate the activities of cells involved in nonspecific defenses (such
bone, although samples are sometimes aspirated from the sternum. In
as phagocytes) and immune responses (such as B cells and T cells).
young children, bone marrow samples are taken from a vertebra or tibia
Two important families of cytokines that stimulate white blood cell
(shin bone). The tissue or cell sample is then sent to a pathology lab for
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analysis. Specifically, laboratory technicians look for signs of neoplastic
formation are colony-stimulating factors (CSFs) and interleukins
(cancer) cells or other diseased cells to assist in diagnosis. (in′-ter-LOO-kins).

Clinical Connection
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In order to form blood cells, pluripotent stem cells in red bone
marrow produce two further types of stem cells, which have the ca- Medical Uses of Hemopoietic Growth Factors
pacity to develop into several types of cells. These stem cells are
called myeloid stem cells and lymphoid stem cells. Myeloid stem Hemopoietic growth factors made available through recombinant DNA
cells begin their development in red bone marrow and give rise to red technology hold tremendous potential for medical uses when a person’s
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natural ability to form new blood cells is diminished or defective. The ar-
blood cells, platelets, monocytes, neutrophils, eosinophils, basophils,
tificial form of erythropoietin (epoetin alfa) is very effective in treating
and mast cells. Lymphoid stem cells, which give rise to lymphocytes,
the diminished red blood cell production that accompanies end-stage
begin their development in red bone marrow but complete it in lym- kidney disease. Granulocyte–macrophage colony-stimulating factor
phatic tissues Lymphoid stem cells also give rise to natural killer (NK) and granulocyte CSF are given to stimulate white blood cell formation in
cells. Although the various stem cells have distinctive cell identity cancer patients who are undergoing chemotherapy, which kills red bone
markers in their plasma membranes, they cannot be distinguished marrow cells as well as cancer cells because both cell types are undergo-
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histologically and resemble lymphocytes. ing mitosis. (Recall that white blood cells help protect against disease.)
During hemopoiesis, some of the myeloid stem cells differenti- Thrombopoietin shows great promise for preventing the depletion of
ate into progenitor cells (prō-JEN-i-tor). Other myeloid stem cells platelets, which are needed to help blood clot, during chemotherapy.
and the lymphoid stem cells develop directly into precursor cells (de- CSFs and thrombopoietin also improve the outcome of patients who
scribed shortly). Progenitor cells are no longer capable of reproduc- receive bone marrow transplants. Hemopoietic growth factors are also
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used to treat thrombocytopenia in neonates, other clotting disorders,
ing themselves and are committed to giving rise to more specific ele-
and various types of anemia.
ments of blood. Some progenitor cells are known as colony-forming
units (CFUs). Following the CFU designation is an abbreviation that
indicates the mature elements in blood that they will produce: CFU–E
ultimately produces erythrocytes (red blood cells); CFU–Meg
y,
produces megakaryocytes, the source of platelets; and CFU–GM ulti- Checkpoint
mately produces granulocytes (specifically, neutrophils) and mono-
cytes (see Figure 19.3). Progenitor cells, like stem cells, resemble 7. Which hemopoietic growth factor regulates differentiation and
lymphocytes and cannot be distinguished by their microscopic proliferation of red blood cell precursors?
appearance alone. 8. Describe the formation of platelets from pluripotent stem cells,
In the next generation, the cells are called precursor cells, also including the influence of hormones.
20
known as blasts. Over several cell divisions they develop into the
actual formed elements of blood. For example, monoblasts devel-
op into monocytes, eosinophilic myeloblasts develop into eosino-
phils, and so on. Precursor cells have recognizable microscopic
appearances. 19.3 Red Blood Cells
Several hormones called hemopoietic growth factors (hē-mō-
20
poy-ET-ik) regulate the differentiation and proliferation of particular
progenitor cells. Erythropoietin (EPO) (e-rith′-rō-POY-ē-tin) increases OBJECTIVE
the number of red blood cell precursors. EPO is produced primarily by
cells in the kidneys that lie between the kidney tubules (peritubular • Describe the structure, functions, life cycle, and production of red
interstitial cells). With renal failure, EPO release slows and RBC pro- blood cells.
duction is inadequate. This leads to a decreased hematocrit, which

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19.3 Red Blood Cells 675

Red blood cells (RBCs) or erythrocytes (e-RITH-rō-sīts; erythro- = red; RBC Physiology
-cyte = cell) contain the oxygen-carrying protein hemoglobin, which
is a pigment that gives whole blood its red color. A healthy adult male Red blood cells are highly specialized for their oxygen transport func-
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has about 5.4 million red blood cells per microliter (μL) of blood,* and tion. Because mature RBCs have no nucleus, all of their internal space
a healthy adult female has about 4.8 million. (One drop of blood is is available for oxygen transport. Because RBCs lack mitochondria
about 50 μL.) To maintain normal numbers of RBCs, new mature cells and generate ATP anaerobically (without oxygen), they do not use up
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must enter the circulation at the astonishing rate of at least 2 million any of the oxygen they transport. Even the shape of an RBC facilitates
per second, a pace that balances the equally high rate of RBC its function. A biconcave disc has a much greater surface area for the
destruction. diffusion of gas molecules into and out of the RBC than would, say, a
sphere or a cube.
Each RBC contains about 280 million hemoglobin molecules. A
RBC Anatomy hemoglobin molecule consists of a protein called globin, composed
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of four polypeptide chains (two alpha and two beta chains); a ringlike
RBCs are biconcave discs with a diameter of 7–8 μm (Figure 19.4a).
nonprotein pigment called a heme (Figure 19.4b) is bound to each of
(Recall that 1 μm = 1/25,000 of an inch or 1/10,000 of a centimeter or
the four chains. At the center of each heme ring is an iron ion (Fe2+)
1/1000 of a millimeter.) Mature red blood cells have a simple struc-
that can combine reversibly with one oxygen molecule (Figure 19.4c),
ture. Their plasma membrane is both strong and flexible, which allows
allowing each hemoglobin molecule to bind four oxygen molecules.
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them to deform without rupturing as they squeeze through narrow
Each oxygen molecule picked up from the lungs is bound to an iron
blood capillaries. As you will see later, certain glycolipids in the
ion. As blood flows through tissue capillaries, the iron–oxygen re-
plasma membrane of RBCs are antigens that account for the various
action reverses. Hemoglobin releases oxygen, which diffuses first into
blood groups such as the ABO and Rh groups. RBCs lack a nucleus and
the interstitial fluid and then into cells.
other organelles and can neither reproduce nor carry on extensive
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Hemoglobin also transports about 23% of the total carbon diox-
metabolic activities. The cytosol of RBCs contains hemoglobin mol-
ide, a waste product of metabolism. (The remaining carbon dioxide is
ecules; these important molecules are synthesized before loss of the
dissolved in plasma or carried as bicarbonate ions.) Blood flowing
nucleus during RBC production and constitute about 33% of the cell’s
through tissue capillaries picks up carbon dioxide, some of which
weight.
combines with amino acids in the globin part of hemoglobin. As blood
flows through the lungs, the carbon dioxide is released from hemo-
*1 μL = 1 mm3 = 10−6 liter. globin and then exhaled.
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ile
FIGURE 19.4 The shapes of a red blood cell (RBC) and a hemoglobin molecule. In (b), note that
each of the four polypeptide chains (blue) of a hemoglobin molecule has one heme group (gold), which
contains an iron ion (Fe2+), shown in red.

The iron portion of a heme group binds oxygen for transport by hemoglobin.
y,
Globins (beta
8 μm polypeptide
CH2
chains)
Heme
H3C CH
C C
2+
Iron (Fe ) HC C C CH
20
H3C N
C C C CH3
C
2+
C N Fe N
C
C C
OOC CH2 N C CH2
Surface view H
CH2 HC C C CH
C C
20
H2 C CH3
Globins (alpha
CH2
Sectioned view polypeptide chains)
OOC
(a) RBC shape (b) Hemoglobin molecule (c) Iron-containing heme

Q How many molecules of O2 can one hemoglobin molecule transport?

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676 CH A PT E R 19 The Cardiovascular System: The Blood

In addition to its key role in transporting oxygen and carbon diox- capillaries. Without a nucleus and other organelles, RBCs cannot syn-
ide, hemoglobin also plays a role in the regulation of blood flow and thesize new components to replace damaged ones. The plasma mem-
blood pressure. The gaseous hormone nitric oxide (NO), produced by brane becomes more fragile with age, and the cells are more likely to
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the endothelial cells that line blood vessels, binds to hemoglobin. Under burst, especially as they squeeze through narrow channels in the
some circumstances, hemoglobin releases NO. The released NO causes spleen. Ruptured red blood cells are removed from circulation and
vasodilation, an increase in blood vessel diameter that occurs when the destroyed by fixed phagocytic macrophages in the spleen and liver,
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smooth muscle in the vessel wall relaxes. Vasodilation improves blood and the breakdown products are recycled and used in numerous met-
flow and enhances oxygen delivery to cells near the site of NO release. abolic processes, including the formation of new red blood cells. The
Red blood cells also contain the enzyme carbonic anhydrase recycling occurs as follows (Figure 19.5):
(CA), which catalyzes the conversion of carbon dioxide and water to
carbonic acid, which in turn dissociates into H+ and HCO3−. The entire 1 Macrophages in the spleen, liver, or red bone marrow phagocytize
reaction is reversible and is summarized as follows: ruptured and worn-out red blood cells.
yr
CA 2 The globin and heme portions of hemoglobin are split apart.
CO2 + H2O H2CO3 H+ + HCO3−
Carbon Water Carbonic Hydrogen Bicarbonate 3 Globin is broken down into amino acids, which can be reused to
dioxide acid ion ion synthesize other proteins.
4 Iron is removed from the heme portion in the form of Fe3+, which
This reaction is significant for two reasons: (1) It allows about 70% of
ig
associates with the plasma protein transferrin (trans-FER-
CO2 to be transported in blood plasma from tissue cells to the lungs in
in; trans- = across; -ferr- = iron), a transporter for Fe3+ in the
the form of HCO3− (see Chapter 23). (2) It also serves as an important
bloodstream.
buffer in extracellular fluid (see Chapter 27).
5 In muscle fibers, liver cells, and macrophages of the spleen and
liver, Fe3+ detaches from transferrin and attaches to an iron-
ht
RBC Life Cycle storage protein called ferritin (FER-i-tin).
Red blood cells live only about 120 days because of the wear and tear 6 On release from a storage site or absorption from the
their plasma membranes undergo as they squeeze through blood gastrointestinal tract, Fe3+ reattaches to transferrin.

FIGURE 19.5 Formation and destruction of red blood cells, and the recycling of hemoglobin
W
components. RBCs circulate for about 120 days after leaving red bone marrow before they are
phagocytized by macrophages.

The rate of RBC formation by red bone marrow equals the rate of RBC destruction by macrophages.
ile

Circulation for about

120 days

3 7

Reused for
y,
Amino +
acids protein synthesis Fe3 Transferrin
Globin
4 6
+ 5
Fe3
3+
2 Heme Ferritin Fe
Transferrin +
Globin
20
Bilirubin
9 +
Biliverdin Bilirubin Liver Vitamin B12
1 Red blood cell 11
death and 10 +
phagocytosis Erythropoietin
Small
Kidney intestine
8 Erythropoiesis in
13 Bilirubin red bone marrow
12
20
Urobilin
Macrophage in Urobilinogen Bacteria Key:
spleen, liver, or
red bone marrow in blood
Stercobilin
Large 14
intestine in bile
Urine Feces

Q What is the function of transferrin?

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19.3 Red Blood Cells 677

7 The Fe3+–transferrin complex is then carried to red bone marrow, mitochondria, ribosomes, and endoplasmic reticulum. They pass
where RBC precursor cells take it up through receptor-mediated from red bone marrow into the bloodstream by squeezing between
endocytosis (see Figure 3.12) for use in hemoglobin synthesis. plasma membranes of adjacent endothelial cells of blood capillaries.
C
Iron is needed for the heme portion of the hemoglobin molecule, Reticulocytes develop into mature red blood cells within 1 to 2 days
and amino acids are needed for the globin portion. Vitamin B12 is after their release from red bone marrow.
also needed for the synthesis of hemoglobin.
op
8 Erythropoiesis in red bone marrow results in the production of Clinical Connection
red blood cells, which enter the circulation.
9 When iron is removed from heme, the non-iron portion of heme Reticulocyte Count
is converted to biliverdin (bil-ē-VER-din), a green pigment, and The rate of erythropoiesis is measured by a reticulocyte count. Nor-
then into bilirubin (bil-ē-ROO-bin), a yellow-orange pigment. mally, a little less than 1% of the oldest RBCs are replaced by newcomer
10 Bilirubin enters the blood and is transported to the liver. reticulocytes on any given day. It then takes 1 to 2 days for the reticu-
yr
locytes to lose the last vestiges of endoplasmic reticulum and become
11 Within the liver, bilirubin is released by liver cells into bile, which
mature RBCs. Thus, reticulocytes account for about 0.5–1.5% of all RBCs
passes into the small intestine and then into the large intestine.
in a normal blood sample. A low “retic” count in a person who is anemic
12 In the large intestine, bacteria convert bilirubin into urobilinogen might indicate a shortage of erythropoietin or an inability of the red bone
(ūr-ō-bī-LIN-ō-jen). marrow to respond to EPO, perhaps because of a nutritional deficiency
ig
13 Some urobilinogen is absorbed back into the blood, converted
or leukemia. A high “retic” count might indicate a good red bone marrow
- response to previous blood loss or to iron therapy in someone who had
to a yellow pigment called urobilin (ūr-ō-BI -lin), and excreted in
been iron-deficient. It could also point to illegal use of epoetin alfa by an
urine.
athlete.
14 Most urobilinogen is eliminated in feces in the form of a brown
ht
-
pigment called stercobilin (ster′-kō-BI -lin), which gives feces its
characteristic color. Normally, erythropoiesis and red blood cell destruction proceed
at roughly the same pace. If the oxygen-carrying capacity of the blood
Clinical Connection falls because erythropoiesis is not keeping up with RBC destruction, a
negative feedback system steps up RBC production (Figure 19.6). The
Iron Overload and Tissue Damage controlled condition is the amount of oxygen delivered to body tissues.
W
An oxygen deficiency at the tissue level, called hypoxia (hī-POKS-ē-a),
Because free iron ions (Fe2+ and Fe3+) bind to and damage molecules in may occur if too little oxygen enters the blood. For example, the lower
cells or in the blood, transferrin and ferritin act as protective “protein es-
oxygen content of air at high altitudes reduces the amount of oxygen in
corts” during transport and storage of iron ions. As a result, plasma con-
the blood. Oxygen delivery may also fall due to anemia, which has
tains virtually no free iron. Furthermore, only small amounts are available
ile
inside body cells for use in synthesis of iron-containing molecules such as
many causes: Lack of iron, lack of certain amino acids, and lack of vita-
the cytochrome pigments needed for ATP production in mitochondria (see min B12 are but a few (see Disorders: Homeostatic Imbalances at the
Figure 25.9). In cases of iron overload, the amount of iron present in the end of this chapter). Circulatory problems that reduce blood flow to
body builds up. Because we have no method for eliminating excess iron, tissues may also reduce oxygen delivery. Whatever the cause, hypoxia
any condition that increases dietary iron absorption can cause iron over- stimulates the kidneys to step up the release of erythropoietin, which
load. At some point, the proteins transferrin and ferritin become saturated speeds the development of proerythroblasts into reticulocytes in the
y,
with iron ions, and free iron level rises. Common consequences of iron red bone marrow. As the number of circulating RBCs increases, more
overload are diseases of the liver, heart, pancreatic islets, and gonads. Iron oxygen can be delivered to body tissues.
overload also allows certain iron-dependent microbes to flourish. Such Premature newborns often exhibit anemia, due in part to inade-
microbes normally are not pathogenic, but they multiply rapidly and can quate production of erythropoietin. During the first weeks after birth,
cause lethal effects in a short time when free iron is present.
the liver, not the kidneys, produces most EPO. Because the liver is less
sensitive than the kidneys to hypoxia, newborns have a smaller EPO
20
response to anemia than do adults. Because fetal hemoglobin (hemo-
globin present at birth) carries up to 30% more oxygen, the loss of
Erythropoiesis: Production of RBCs fetal hemoglobin, due to insufficient erythropoietin production,
makes the anemia worse.
Erythropoiesis (e-rith′-rō-poy-Ē-sis), the production of RBCs, starts
in the red bone marrow with a precursor cell called a proerythroblast
20
(prō-e-RITH-rō-blast) (see Figure 19.3). The proerythroblast divides Clinical Connection
several times, producing cells that begin to synthesize hemoglobin.
Ultimately, a cell near the end of the development sequence ejects its Blood Doping
nucleus and becomes a reticulocyte (re-TIK-ū-lō-sīt). Loss of the Delivery of oxygen to muscles is a limiting factor in muscular feats from
nucleus causes the center of the cell to indent, producing the red weightlifting to running a marathon. As a result, increasing the oxygen-
blood cell’s distinctive biconcave shape. Reticulocytes retain some carrying capacity of the blood enhances athletic performance, especially

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678 CH A PT E R 19 The Cardiovascular System: The Blood

FIGURE 19.6 Negative feedback regulation of erythropoiesis (red in endurance events. Because RBCs transport oxygen, athletes have tried
blood cell formation). Lower oxygen content of air at high altitudes, several means of increasing their RBC count, known as blood doping or
anemia, and circulatory problems may reduce oxygen delivery to body artificially induced polycythemia (an abnormally high number of RBCs),
C
tissues. to gain a competitive edge. Athletes have enhanced their RBC production
by injecting epoetin alfa (Procrit® or Epogen®), a drug that is used to treat
The main stimulus for erythropoiesis is hypoxia, an oxygen deficiency anemia by stimulating the production of RBCs by red bone marrow. Prac-
at the tissue level.
op
tices that increase the number of RBCs are dangerous because they raise
the viscosity of the blood, which increases the resistance to blood flow and
makes the blood more difficult for the heart to pump. Increased viscosity
also contributes to high blood pressure and increased risk of stroke. Dur-
STIMULUS ing the 1980s, at least 15 competitive cyclists died from heart attacks or
strokes linked to suspected use of epoetin alfa. Although the International
Olympics Committee bans the use of epoetin alfa, enforcement is difficult
yr
Disrupts homeostasis
by decreasing because the drug is identical to naturally occurring erythropoietin (EPO).
So-called natural blood doping is seemingly the key to the success
of marathon runners from Kenya. The average altitude throughout
CONTROLLED CONDITION Kenya’s highlands is about 6000 feet (1829 meters) above sea level;
Oxygen delivery to kidneys other areas of Kenya are even higher. Altitude training greatly improves
ig
(and other tissues) fitness, endurance, and performance. At these higher altitudes, the body
increases the production of red blood cells, which means that exercise
greatly oxygenates the blood. When these runners compete in Boston,
for example, at an altitude just above sea level, their bodies contain more
ht
erythrocytes than do the bodies of competitors who trained in Boston. A
RECEPTORS
number of training camps have been established in Kenya and now attract
Kidney cells endurance athletes from all over the world.

–
Detect low oxygen levels,
Input increasing erythropoietin
W
secretion into blood Checkpoint
9. Describe the size, microscopic appearance, and functions of RBCs.
CONTROL CENTER
10. How is hemoglobin recycled?
Proerythroblasts
Return to
in red bone 11. What is erythropoiesis? How does erythropoiesis affect
ile
homeostasis when
marrow mature
oxygen delivery to hematocrit? What factors speed up and slow down
more quickly
kidneys increases erythropoiesis?
into reticulocytes
to normal

Output More reticulocytes

enter circulating blood
White Blood Cells
y,
19.4
EFFECTORS
Larger number
of red blood cells OBJECTIVE
in circulation
• Describe the structure, functions, and production of white blood
20
cells.

RESPONSE
Increased oxygen
delivery to tissues
Types of White Blood Cells
20
Unlike red blood cells, white blood cells (WBCs) or leukocytes (LOO-
kō-sīts; leuko- = white) have nuclei and a full complement of other
Q How might your hematocrit change if you moved from a organelles but they do not contain hemoglobin. WBCs are classified
town at sea level to a high mountain village?
as either granular or agranular, depending on whether they contain
conspicuous chemical-filled cytoplasmic granules (vesicles) that are
made visible by staining when viewed through a light microscope.

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19.4 White Blood Cells 679

Granular leukocytes include neutrophils, eosinophils, and basophils; cell, the more cytoplasm is visible. Lymphocytes are classified by
agranular leukocytes include lymphocytes and monocytes. As shown cell diameter as large lymphocytes (10–14 μm) or small lymphocytes
in Figure 19.3, monocytes and granular leukocytes develop from (6–9 μm). Although the functional significance of the size difference
C
myeloid stem cells. In contrast, lymphocytes develop from lymphoid between small and large lymphocytes is unclear, the distinction is
stem cells. still clinically useful because an increase in the number of large lym-
phocytes has diagnostic significance in acute viral infections and in
op
Granular Leukocytes After staining, each of the three types some immunodeficiency diseases.
of granular leukocytes displays conspicuous granules with distinctive • Monocyte. The nucleus of monocyte
a (MON-ō-sīt′) is usually
coloration that can be recognized under a light microscope. Granular kidney-shapedor horseshoe-shaped, and the cytoplasm is blue-gray
leukocytes can be distinguished as follows: and has a foamy appearance (Figure 19.7e). The cytoplasm’s color
• Neutrophil. The granules of a neutrophil (NOO-trō-fil) are smaller and appearance are due to very fine azurophilic granules (az′-ū-rō-
than those of other granular leukocytes, evenly distributed, and pale FIL-ik; azur- = blue; -philic = loving), which are lysosomes. Blood is
yr
lilac (Figure 19.7a). Because the granules do not strongly attract merely a conduit for monocytes, which migrate from the blood into
either the acidic (red) or basic (blue) stain, these WBCs are neutro- the tissues, where they enlarge and differentiate into macrophages
philic (= neutral loving). The nucleus has two to five lobes, con- (MAK-rō-fā-jez = large eaters). Some become fixed (tissue) mac-
nected by very thin strands of nuclear material. As the cells age, the rophages, which means they reside in a particular tissue; examples
ig
number of nuclear lobes increases. Because older neutrophils thus are alveolar macrophages in the lungsor macrophages in the spleen.
have several differently shaped nuclear lobes, they are often called Others become wandering macrophages, which roam the tissues
polymorphonuclear leukocytes (PMNs), polymorphs, or “polys.” and gather at sites of infection or inflammation.
• Eosinophil. The large, uniform-sized granules within an eosinophil White blood cells and all other nucleated cells in the body have
(ē-ō-SIN-ō-fil) are eosinophilic (= eosin-loving)—they stain red- proteins, called major histocompatibility (MHC) antigens, protrud-
ht
orange with acidic dyes (Figure 19.7b). The granules usually do not ing from their plasma membrane into the extracellular fluid. These
cover or obscure the nucleus, which most often has two lobes con- “cell identity markers” are unique for each person (except identical
nected by either a thin strand or a thick strand of nuclear material. twins). Although RBCs possess blood group antigens, they lack the
• Basophil. The round, variable-sized granules of a basophil (BĀ-sō- MHC antigens.
fil) are basophilic (= basic loving)—they stain blue-purple with basic
dyes (Figure 19.7c). The granules commonly obscure the nucleus,
Functions of White Blood Cells
W
which has two lobes. In a healthy body, some WBCs, especially lymphocytes, can live for
several months or years, but most live only a few days. During a
period of infection, phagocytic WBCs may live only a few hours. WBCs
Agranular Leukocytes Even though so-called agranular
leukocytes possess cytoplasmic granules, the granules are not visible are far less numerous than red blood cells; at about 5000–10,000 cells
ile
under a light microscope because of their small size and poor staining per microliter of blood, they are outnumbered by RBCs by about
qualities. 700:1. Leukocytosis (loo′-kō-sī-TO-sis),
- an increase in the number of
WBCs above 10,000/μL, is a normal, protective response to stresses
• Lymphocyte. The nucleus of a lymphocyte (LIM-fō-sīt) stains dark
such as invading microbes, strenuous exercise, anesthesia, and
and is round or slightly indented (Figure 19.7d). The cytoplasm
surgery. An abnormally low level of white blood cells (below 5000/μL)
stains sky blue and forms a rim around the nucleus. The larger the
is termed
y,
FIGURE 19.7 Types of white blood cells.

The shapes of their nuclei and the staining properties of their cytoplasmic granules distinguish
white blood cells from one another.
20
20

Courtesy Michael Ross, University of Florida LM all 1600x

(a) Neutrophil (b) Eosinophil (c) Basophil (d) Lymphocyte (e) Monocyte

Q Which WBCs are called granular leukocytes? Why?

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680 CHAPTER 19 The Cardiovascular System: The Blood

leukopenia (loo′-kō-PĒ-nē-a). It is never beneficial and may be FIGURE 19.8 Emigration of white blood cells.
caused by radiation, shock, and certain chemotherapeutic agents.
The skin and mucous membranes of the body are continuously Adhesion molecules (selectins and integrins) assist the emigration of
C
exposed to microbes and their toxins. Some of these microbes can WBCs from the bloodstream into interstitial fluid.
invade deeper tissues to cause disease. Once pathogens enter the
body, the general function of white blood cells is to combat them by
op
phagocytosis or immune responses. To accomplish these tasks, many
Interstitial fluid
WBCs leave the bloodstream and collect at sites of pathogen invasion
or inflammation. Once granular leukocytes and monocytes leave the Blood flow
bloodstream to fight injury or infection, they never return to it. Lym-
phocytes, on the other hand, continually recirculate—from blood to
interstitial spaces of tissues to lymphatic fluid and back to blood. Only Neutrophil
yr
2% of the total lymphocyte population is circulating in the blood at
Endothelial cell
any given time; the rest is in lymphatic fluid and organs such as the
Emigration
skin, lungs, lymph nodes, and spleen. Rolling
RBCs are contained within the bloodstream, but WBCs leave the
bloodstream by a process termed emigration (em′-i-GRĀ-shun; e- =
ig
out; -migra- = wander), also called diapedesis (dī-a-pe-DĒ-sis), in
Sticking
which they roll along the endothelium, stick to it, and then squeeze
between endothelial cells (Figure 19.8). The precise signals that
stimulate emigration through a particular blood vessel vary for the
ht
diff e rent types of WBCs. Molecules k nown a s a dhesion molecules Squeezing between
help WBCs stick to the endothelium. For example, endothelial cells endothelial cells
display adhesion molecules called selectins in response to nearby in-
jury and inflammation. Selectins stick to carbohydrates on the sur- Key:
face of neutrophils, causing them to slow down and roll along the en- Selectins on
dothelial surface. On the neutrophil surface are other adhesion endothelial cells
molecules called integrins, which tether neutrophils to the endotheli- Integrins on
W
um and assist their movement through the blood vessel wall and into neutrophil
the interstitial fluid of the injured tissue.
Neutrophils and macrophages are active in phagocytosis (fag′- Q In what way is the “traffic pattern” of lymphocytes in the
- body different from that of other WBCs?
ō-sī-TO-sis); they can ingest bacteria and dispose of dead matter (see
ile
Figure 3.13). Several diff e rent chemicals r eleased b y m icrobes a nd
inflamed tissues attract phagocytes, a phenomenon called chemo-
taxis (kē-mō-TAK-sis). The substances that provide stimuli for antibody complexes and are effective against certain parasitic worms.
chemotaxis include toxins produced by microbes; kinins, which are A high eosinophil count often indicates an allergic condition or a para-
specialized products of damaged tissues; and some of the colony- sitic infection.
stimulating factors (CSFs). The CSFs also enhance the phagocytic At sites of inflammation, basophils leave capillaries, enter tissues,
y,
activity of neutrophils and macrophages. and release granules that contain heparin, histamine, and serotonin.
Among WBCs, neutrophils respond most quickly to tissue de- These substances intensify the inflammatory reaction and are in-
struction by bacteria. Aft er engulfing a pathogen during phagocytosis, volved in hypersensitivity (allergic) reactions. Basophils are similar in
a neutrophil unleashes several chemicals to destroy the pathogen. function to mast cells, connective tissue cells that originate from
- pluripotent stem cells in red bone marrow. Like basophils, mast cells
These chemicals include the enzyme lysozyme (LI -sō-zīm), which de-
stroys certain bacteria, and strong oxidants, such as the superoxide release substances involved in inflammation, including heparin,
20
anion (O2−), hydrogen peroxide (H2O2), and the hypochlorite anion histamine, and proteases. Mast cells are widely dispersed in the body,
(OCl−), which is similar to household bleach. Neutrophils also contain particularly in connective tissues of the skin and mucous membranes
defensins, proteins that exhibit a broad range of antibiotic activity of the respiratory and gastrointestinal tracts.
against bacteria and fungi. Within a neutrophil, vesicles containing Lymphocytes are the major soldiers in lymphatic system battles
defensins merge with phagosomes containing microbes. Defensins (described in detail in Chapter 22). Most lymphocytes continually
form peptide “spears” that poke holes in microbe membranes; the move among lymphoid tissues, lymph, and blood, spending only a
20
resulting loss of cellular contents kills the invader. few hours at a time in blood. Thus, only a small proportion of the total
Eosinophils leave the capillaries and enter tissue fluid. They are lymphocytes are present in the blood at any given time. Three main
believed to release enzymes, such as histaminase, that combat the types of lymphocytes are B cells, T cells, and natural killer (NK) cells.
eff ects of histamine and other substances involved in inflammation B cells are particularly effective in destroying bacteria and inactivat-
during allergic reactions. Eosinophils also phagocytize antigen– ing their toxins. T cells attack infected body cells and tumor cells, and

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19.5 Platelets 681

are responsible for the rejection of transplanted organs. Immune re-

Checkpoint
sponses carried out by both B cells and T cells help combat infection
and provide protection against some diseases. Natural killer cells at- 12. What is the importance of emigration, chemotaxis, and
C
tack a wide variety of infected body cells and certain tumor cells. phagocytosis in fighting bacterial invaders?
Monocytes take longer to reach a site of infection than neutro- 13. How are leukocytosis and leukopenia different?
phils, but they arrive in larger numbers and destroy more microbes.
14. What is a differential white blood cell count?
op
On their arrival, monocytes enlarge and differentiate into wandering
macrophages, which clean up cellular debris and microbes by phago- 15. What functions do granular leukocytes, macrophages, B cells,
cytosis after an infection. T cells, and natural killer cells perform?
As you have already learned, an increase in the number of circu-
lating WBCs usually indicates inflammation or infection. A physician
may order a differential white blood cell count, or “diff”, a count of 19.5 Platelets
yr
each of the five types of white blood cells, to detect infection or in-
flammation, determine the effects of possible poisoning by chemicals
or drugs, monitor blood disorders (for example, leukemia) and the
effects of chemotherapy, or detect allergic reactions and parasitic OBJECTIVE
infections. Because each type of white blood cell plays a different role,
ig
determining the percentage of each type in the blood assists in diag- • Describe the structure, function, and origin of platelets.
nosing the condition. Table 19.2 lists the significance of both high
and low WBC counts.
Besides the immature cell types that develop into erythrocytes and
leukocytes, hemopoietic stem cells also differentiate into cells that
ht
produce platelets. Under the influence of the hormone thrombo-
poietin, myeloid stem cells develop into megakaryocyte colony-
forming cells that in turn develop into precursor cells called
megakaryoblasts (see Figure 19.3). Megakaryoblasts transform into
megakaryocytes, huge cells that splinter into 2000 to 3000 fragments.
TA B LE 1 9 . 2 Significance of High and Low White Blood Cell Counts Each fragment, enclosed by a piece of the plasma membrane, is a
W
HIGH COUNT LOW COUNT MAY platelet. Platelets break off from the megakaryocytes in red bone mar-
WBC TYPE MAY INDICATE INDICATE row and then enter the blood circulation. Between 150,000 and 400,000
platelets are present in each microliter of blood. Each is irregularly disc-
Neutrophils Bacterial infection, Radiation exposure,
burns, stress, drug toxicity, shaped, 2–4 μm in diameter, and has many vesicles but no nucleus.
Their granules contain chemicals that, once released, promote
ile
inflammation. vitamin B12 deficiency,
systemic lupus blood clotting. Platelets help stop blood loss from damaged blood
erythematosus (SLE). vessels by forming a platelet plug. Platelets have a short life span, nor-
mally just 5 to 9 days. Aged and dead platelets are removed by fixed
Lymphocytes Viral infections, some Prolonged illness,
leukemias, infectious HIV infection, macrophages in the spleen and liver.
mononucleosis. immunosuppression, Table 19.3 summarizes the formed elements in blood.
Courtesy Michael Ross, University of Florida

treatment with
y,
cortisol. Clinical Connection
Monocytes Viral or fungal Bone marrow
infections, tuberculosis, suppression, Complete Blood Count
some leukemias, other treatment with
chronic diseases. cortisol. A complete blood count (CBC) is a very valuable test that screens for ane-
mia and various infections. Usually included are counts of RBCs, WBCs, and
20
platelets per microliter of whole blood; hematocrit; and differential white
blood cell count. The amount of hemoglobin in grams per milliliter of blood
Eosinophils Allergic reactions, Drug toxicity, stress,
also is determined. Normal hemoglobin ranges are as follows: infants, 14–
parasitic infections, acute allergic
20 g/100 mL of blood; adult females, 12–16 g/100 mL of blood; and adult
autoimmune diseases. reactions.
males, 13.5–18 g/100 mL of blood.
20
Basophils Allergic reactions, Pregnancy,
leukemias, cancers, ovulation, stress, Checkpoint
hypothyroidism. hypothyroidism.
16. How do RBCs, WBCs, and platelets compare with respect to size,
number per microliter of blood, and life span?

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682 CH A PT E R 19 The Cardiovascular System: The Blood

TA B L E 1 9 . 3 Summary of Formed Elements in Blood

NAME AND APPEARANCE NUMBER CHARACTERISTICS* FUNCTIONS

C

RED BLOOD CELLS (RBCS) OR 4.8 million/μL in females; 7–8 μm diameter, biconcave discs, Hemoglobin within RBCs transports
ERYTHROCYTES 5.4 million/μL in males. without nuclei; live for about most oxygen and part of carbon
120 days. dioxide in blood.
op

Juergen Berger/Science Source Images

WHITE BLOOD CELLS (WBCS) 5000–10,000/μL. Most live for a few hours to a few Combat pathogens and other foreign
OR LEUKOCYTES days.† substances that enter body.
Granular leukocytes
yr
Neutrophils 60–70% of all WBCs. 10–12 μm diameter; nucleus has Phagocytosis. Destruction of bacteria
2–5 lobes connected by thin strands with lysozyme, defensins, and strong
of chromatin; cytoplasm has very oxidants, such as superoxide anion,
fine, pale lilac granules. hydrogen peroxide, and hypochlorite
Courtesy Michael Ross, University of Florida

anion.
ig
Eosinophils 2–4% of all WBCs. 10–12 μm diameter; nucleus usually Combat effects of histamine in allergic
has 2 lobes connected by thick reactions, phagocytize antigen–
strand of chromatin; large, red- antibody complexes, and destroy
orange granules fill cytoplasm. certain parasitic worms.
ht

Basophils 0.5–1% of all WBCs. 8–10 μm diameter; nucleus has Liberate heparin, histamine, and
2 lobes; large cytoplasmic granules serotonin in allergic reactions that
appear deep blue-purple. intensify overall inflammatory
response.

Agranular leukocytes
W
Lymphocytes (T cells, 20–25% of all WBCs. Small lymphocytes are 6–9 μm in Mediate immune responses, including
B cells, and natural diameter; large lymphocytes are antigen–antibody reactions. B cells
killer cells) 10–14 μm in diameter; nucleus develop into plasma cells, which
is round or slightly indented; secrete antibodies. T cells attack
Courtesy Michael Ross, University of Florida

cytoplasm forms rim around invading viruses, cancer cells, and

ile
nucleus that looks sky blue; the transplanted tissue cells. Natural killer
larger the cell, the more cytoplasm cells attack wide variety of infectious
is visible. microbes and certain spontaneously
arising tumor cells.
Monocytes 3–8% of all WBCs. 12–20 μm diameter; nucleus is Phagocytosis (after transforming into
kidney-or horseshoe-shaped; fixed or wandering macrophages).
cytoplasm is blue-gray and appears
y,
foamy.

PLATELETS 150,000–400,000/μL. 2–4 μm diameter cell fragments Form platelet plug in hemostasis;
that live for 5–9 days; contain many release chemicals that promote
20
vesicles but no nucleus. vascular spasm and blood clotting.
Mark Nielsen

*Colors are those seen when using Wright’s stain.

†
Some lymphocytes, called T and B memory cells, can live for many years once they are established.
20

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19.7 Hemostasis 683

3. They are less likely to cause graft-versus-host disease, so the match

19.6 Stem Cell Transplants from between donor and recipient does not have to be as close as in a
bone marrow transplant. This provides a larger number of poten-
Bone Marrow and Cord Blood
C
tial donors.
4. They are less likely to transmit infections.
OBJECTIVE 5. They can be stored indefinitely in cord-blood banks.
op

• Explain the importance of bone marrow transplants and stem cell

Checkpoint
transplants.
17. How are cord-blood transplants and bone marrow transplants
similar? How do they differ?
A bone marrow transplant is the replacement of cancerous or abnormal
yr
red bone marrow with healthy red bone marrow in order to establish nor-
mal blood cell counts. In patients with cancer or certain genetic diseases,
the defective red bone marrow is destroyed by high doses of chemother- 19.7 Hemostasis
apy and whole body radiation just before the transplant takes place.
These treatments kill the cancer cells and destroy the patient’s immune
ig
system in order to decrease the chance of transplant rejection. OBJECTIVES
Healthy red bone marrow for transplanting may be supplied by a
donor or by the patient when the underlying disease is inactive, as • Describe the three mechanisms that contribute to hemostasis.
when leukemia is in remission. The red bone marrow from a donor is • Explain the various factors that promote and inhibit blood clotting.
ht
usually removed from the iliac crest of the hip bone under general an-
esthesia with a syringe and is then injected into the recipient’s vein,
much like a blood transfusion. The injected marrow migrates to the Hemostasis (hē-mō-STĀ-sis), not to be confused with the very similar
recipient’s red bone marrow cavities, where the donor’s stem cells term homeostasis, is a sequence of responses that stops bleeding.
multiply. If all goes well, the recipient’s red bone marrow is replaced When blood vessels are damaged or ruptured, the hemostatic
entirely by healthy, noncancerous cells. response must be quick, localized to the region of damage, and care-
W
Bone marrow transplants have been used to treat aplastic anemia, fully controlled in order to be effective. Three mechanisms reduce
certain types of leukemia, severe combined immunodeficiency disease blood loss: (1) vascular spasm, (2) platelet plug formation, and
(SCID), Hodgkin’s disease, non-Hodgkin’s lymphoma, multiple myelo- (3) blood clotting (coagulation). When successful, hemostasis pre-
ma, thalassemia, sickle-cell disease, breast cancer, ovarian cancer, tes- vents hemorrhage (HEM-o-rij; -rhage = burst forth), the loss of a large
ticular cancer, and hemolytic anemia. However, there are some draw- amount of blood from the vessels. Hemostatic mechanisms can pre-
ile
backs. Since the recipient’s white blood cells have been completely vent hemorrhage from smaller blood vessels, but extensive hemor-
destroyed by chemotherapy and radiation, the patient is extremely rhage from larger vessels usually requires medical intervention.
vulnerable to infection. (It takes about 2–3 weeks for transplanted bone
marrow to produce enough white blood cells to protect against infec-
tion.) In addition, transplanted red bone marrow may produce T cells
Vascular Spasm
that attack the recipient’s tissues, a reaction called graft-versus-host
y,
When arteries or arterioles are damaged, the circularly arranged
disease. Similarly, any of the recipient’s T cells that survived the chemo- smooth muscle in their walls contracts immediately, a reaction called
therapy and radiation can attack donor transplant cells. Another draw- vascular spasm. This reduces blood loss for several minutes to sev-
back is that patients must take immunosuppressive drugs for life. Be- eral hours, during which time the other hemostatic mechanisms go
cause these drugs reduce the level of immune system activity, they into operation. The spasm is probably caused by damage to the
increase the risk of infection. Immunosuppressive drugs also have side smooth muscle, by substances released from activated platelets, and
20
effects such as fever, muscle aches, headache, nausea, fatigue, depres- by reflexes initiated by pain receptors.
sion, high blood pressure, and kidney and liver damage.
A more recent advance for obtaining stem cells involves a cord-
blood transplant. The connection between the mother and embryo
Platelet Plug Formation
(and later the fetus) is the umbilical cord. Stem cells may be obtained Considering their small size, platelets store an impressive array of
from the umbilical cord shortly after birth. The stem cells are removed chemicals. Within many vesicles are clotting factors, ADP, ATP, Ca2+,
20
from the cord with a syringe and then frozen. Stem cells from the cord and serotonin. Also present are enzymes that produce thromboxane
have several advantages over those obtained from red bone marrow: A2, a prostaglandin; fibrin-stabilizing factor, which helps to strengthen
a blood clot; lysosomes; some mitochondria; membrane systems that
1. They are easily collected following permission of the newborn’s take up and store calcium and provide channels for release of the
parents. contents of granules; and glycogen. Also within platelets is
2. They are more abundant than stem cells in red bone marrow. platelet-derived growth factor (PDGF), a hormone that can cause

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684 CH A PT E R 19 The Cardiovascular System: The Blood

proliferation of vascular endothelial cells, vascular smooth muscle 2 Due to adhesion, the platelets become activated, and their
fibers, and fibroblasts to help repair damaged blood vessel walls. characteristics change dramatically. They extend many projections
Platelet plug formation occurs as follows (Figure 19.9): that enable them to contact and interact with one another, and
C
1 Initially, platelets contact and stick to parts of a damaged blood they begin to liberate the contents of their vesicles. This phase
vessel, such as collagen fibers of the connective tissue underlying the is called the platelet release reaction. Liberated ADP and
damaged endothelial cells. This process is called platelet adhesion. thromboxane A2 play a major role by activating nearby platelets.
op
Serotonin and thromboxane A2 function as vasoconstrictors,
causing and sustaining contraction of vascular smooth muscle,
FIGURE 19.9 Platelet plug formation. which decreases blood flow through the injured vessel.
3 The release of ADP makes other platelets in the area sticky, and
A platelet plug can stop blood loss completely if the hole in a blood the stickiness of the newly recruited and activated platelets
vessel is small enough. causes them to adhere to the originally activated platelets. This
yr
gathering of platelets is called platelet aggregation. Eventually,
Red blood cell the accumulation and attachment of large numbers of platelets
Platelet form a mass called a platelet plug.
A platelet plug is very effective in preventing blood loss in a small
ig
vessel. Although initially the platelet plug is loose, it becomes quite
tight when reinforced by fibrin threads formed during clotting (see
Figure 19.10). A platelet plug can stop blood loss completely if the
hole in a blood vessel is not too large.
ht
Collagen fibers
and damaged FIGURE 19.10 Blood clot formation. Notice the platelet and red blood
endothelium cells entrapped in fibrin threads.

A blood clot is a gel that contains formed elements of the blood

1 Platelet adhesion entangled in fibrin threads.
W
Collagen
fibers Platelet

Erythrocyte
ile
Fibrin threads

Susumu Nishinaga/Science SEM 900x

Source Images
(a) Early stage
Liberated ADP,
serotonin, and
Steve Gschmeissner/Science

thromboxane A2
y,

2 Platelet release reaction

Collagen
Source

fibers
SEM 900x
20
(b) Intermediate stage

Blood
vessel
Fibrin
threads Blood
dot
Erythrocyte
20

PLATELET PLUG
Steve Gschmeissner/Science SEM 900x MOREDUN ANIMAL SEM 30x
Source HEALTH LTD/Getty Images
3 Platelet aggregation (c) Late stage showing red blood
cells trapped in fibrin threads
Q Along with platelet plug formation, which two
mechanisms contribute to hemostasis? Q What is serum?

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19.7 Hemostasis 685

Blood Clotting FIGURE 19.11 The blood-clotting cascade. Green arrows represent
positive feedback cycles.
Normally, blood remains in its liquid form as long as it stays within its
C
vessels. If it is drawn from the body, however, it thickens and forms a In blood clotting, coagulation factors are activated in sequence, resulting
gel. Eventually, the gel separates from the liquid. The straw-colored liq- in a cascade of reactions that includes positive feedback cycles.
uid, called serum, is simply blood plasma minus the clotting proteins.
op
The gel is called a blood clot. It consists of a network of insoluble pro-
tein fibers called fibrin in which the formed elements of blood are (a) EXTRINSIC PATHWAY (b) INTRINSIC PATHWAY
trapped (Figure 19.10).
Tissue trauma Blood trauma
The process of gel formation, called clotting or coagulation
-
(kō-ag-u-LA -shun), is a series of chemical reactions that culminates Damaged
in formation of fibrin threads. If blood clots too easily, the result endothelial cells
- expose collagen
yr
can be thrombosis (throm-BO-sis; thromb- = clot; -osis = a condi- fibers
tion of)—clotting in an undamaged blood vessel. If the blood takes
Tissue
too long to clot, hemorrhage can occur. factor
Clotting involves several substances known as clotting (coagula- (TF)
tion) factors. These factors include calcium ions (Ca2+), several inactive
ig
enzymes that are synthesized by hepatocytes (liver cells) and released Damaged
into the bloodstream, and various molecules associated with platelets platelets
or released by damaged tissues. Most clotting factors are identified by
Roman numerals that indicate the order of their discovery (not neces-
Activated XII
ht
sarily the order of their participation in the clotting process).
Clotting is a complex cascade of enzymatic reactions in which each Activated
2+
clotting factor activates many molecules of the next one in a fixed se- Ca2+ Ca platelets
quence. Finally, a large quantity of product (the insoluble protein fibrin) +
is formed. Clotting can be divided into three stages (Figure 19.11):
Platelet
phospholipids
1 Two pathways, called the extrinsic pathway and the intrinsic
W
pathway (Figures 19.11a, b), which will be described shortly,
lead to the formation of prothrombinase. Once prothrombinase Activated X Activated X
is formed, the steps involved in the next two stages of clotting
V V +
are the same for both the extrinsic and intrinsic pathways, and Ca2+ Ca2+
together these two stages are referred to as the common pathway. 1 PROTHROMBINASE
ile
2 Prothrombinase converts prothrombin (a plasma protein formed (c) COMMON
by the liver) into the enzyme thrombin. PATHWAY
2+
3 Thrombin converts soluble fibrinogen (another plasma protein Ca
formed by the liver) into insoluble fibrin. Fibrin forms the threads Prothrombin
(II)
of the clot. THROMBIN 2
y,
2+
Ca XIII
The Extrinsic Pathway The extrinsic pathway of blood
Fibrinogen
clotting has fewer steps than the intrinsic pathway and occurs (I) Activated XIII
rapidly—within a matter of seconds if trauma is severe. It is so named
Loose fibrin STRENGTHENED
because a tissue protein called tissue factor (TF), also known as 3
threads FIBRIN THREADS
20
thromboplastin (throm′-bō-PLAS-tin), leaks into the blood from
cells outside (extrinsic to) blood vessels and initiates the formation
of prothrombinase. TF is a complex mixture of lipoproteins and
phospholipids released from the surfaces of damaged cells. In the
presence of Ca2+, TF begins a sequence of reactions that ultimately
activates clotting factor X (Figure 19.11a). Once factor X is activated,
Q What is the outcome of the first stage of blood clotting?
20
it combines with factor V in the presence of Ca2+ to form the active
enzyme prothrombinase, completing the extrinsic pathway. contained within (intrinsic to) the blood; outside tissue damage is not
needed. If endothelial cells become roughened or damaged, blood can
The Intrinsic Pathway The intrinsic pathway of blood come in contact with collagen fibers in the connective tissue around the
clotting is more complex than the extrinsic pathway, and it occurs more endothelium of the blood vessel. In addition, trauma to endothelial cells
slowly, usually requiring several minutes. The intrinsic pathway is so causes damage to platelets, resulting in the release of phospholipids
named because its activators are either in direct contact with blood or by the platelets. Contact with collagen fibers (or with the glass sides

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686 CH A PT E R 19 The Cardiovascular System: The Blood

of a blood collection tube) activates clotting factor XII (Figure 19.11b), which release factor XIII and other factors, thereby strengthening and
which begins a sequence of reactions that eventually activates clotting stabilizing the clot. Permanent repair of the blood vessel can then
factor X. Platelet phospholipids and Ca2+ can also participate in the take place. In time, fibroblasts form connective tissue in the ruptured
C
activation of factor X. Once factor X is activated, it combines with factor area, and new endothelial cells repair the vessel lining.
V to form the active enzyme prothrombinase (just as occurs in the
extrinsic pathway), completing the intrinsic pathway. Role of Vitamin K in Clotting
op

The Common Pathway The formation of prothrombinase Normal clotting depends on adequate levels of vitamin K in the body.
marks the beginning of the common pathway. In the second stage of Although vitamin K is not involved in actual clot formation, it is
blood clotting (Figure 19.11c), prothrombinase and Ca2+ catalyze the required for the synthesis of four clotting factors. Normally produced
conversion of prothrombin to thrombin. In the third stage, thrombin, by bacteria that inhabit the large intestine, vitamin K is a fat-soluble
in the presence of Ca2+, converts fibrinogen, which is soluble, to loose vitamin that can be absorbed through the lining of the intestine and
yr
fibrin threads, which are insoluble. Thrombin also activates factor XIII into the blood if absorption of lipids is normal. People suffering from
(fibrin stabilizing factor), which strengthens and stabilizes the fibrin disorders that slow absorption of lipids (for example, inadequate
threads into a sturdy clot. Plasma contains some factor XIII, which is release of bile into the small intestine) oft en experience uncontrolled
also released by platelets trapped in the clot. bleeding as a consequence of vitamin K deficiency.
Thrombin has two positive feedback effects. In the first positive The various clotting factors, their sources, and the pathways of
ig
feedback loop, which involves factor V, it accelerates the formation of activation are summarized in Table 19.4.
prothrombinase. Prothrombinase in turn accelerates the production
of more thrombin, and so on. In the second positive feedback loop,
thrombin activates platelets, which reinforces their aggregation and
Homeostatic Control Mechanisms
ht
the release of platelet phospholipids. Many times a day little clots start to form, oft en at a site of minor rough-
ness or at a developing atherosclerotic plaque inside a blood vessel.
Clot Retraction Once a clot is formed, it plugs the ruptured Because blood clotting involves amplification and positive feedback
area of the blood vessel and thus stops blood loss. Clot retraction cycles, a clot has a tendency to enlarge, creating the potential for impair-
is the consolidation or tightening of the fibrin clot. The fibrin threads ment of blood flow through undamaged vessels. The fibrinolytic system
attached to the damaged surfaces of the blood vessel gradually (fī-bri-nō-LIT-ik) dissolves small, inappropriate clots; it also dissolves clots
contract as platelets pull on them. As the clot retracts, it pulls the at a site of damage once the damage is repaired. Dissolution of a clot is
W
edges of the damaged vessel closer together, decreasing the risk of called fibrinolysis (fī-bri-NOL-i-sis). When a clot is formed, an inactive
further damage. During retraction, some serum can escape between plasma enzyme called plasminogen (plaz-MIN-o-jen) is incorporated into
the fibrin threads, but the formed elements in blood cannot. Normal the clot. Both body tissues and blood contain substances that can
retraction depends on an adequate number of platelets in the clot, -
activate plasminogen to plasmin or fibrinolysin (fī-brin-ō-LI-sin), an active
ile
plasma

TA B L E 1 9 . 4 Clotting (Coagulation) Factors

PATHWAY(S) OF
NUMBER* NAME(S) SOURCE ACTIVATION
y,
I Fibrinogen. Liver. Common.
II Prothrombin. Liver. Common.
III Tissue factor (thromboplastin). Damaged tissues and activated platelets. Extrinsic.
IV Calcium ions (Ca2+). Diet, bones, and platelets. All.
V Proaccelerin, labile factor, or accelerator globulin (AcG). Liver and platelets. Extrinsic and
intrinsic.
20
VII Serum prothrombin conversion accelerator (SPCA), stable factor, or Liver. Extrinsic.
proconvertin.
VIII Antihemophilic factor (AHF), antihemophilic factor A, or antihemophilic Liver. Intrinsic.
globulin (AHG).
IX Christmas factor, plasma thromboplastin component (PTC), or Liver. Intrinsic.
antihemophilic factor B.
20
X Stuart factor, Prower factor, or thrombokinase. Liver. Extrinsic and intrinsic.
XI Plasma thromboplastin antecedent (PTA) or antihemophilic factor C. Liver. Intrinsic.
XII Hageman factor, glass factor, contact factor, or antihemophilic factor D. Liver. Intrinsic.
XIII Fibrin-stabilizing factor (FSF). Liver and platelets. Common.

*There is no factor VI. Prothrombinase (prothrombin activator) is a combination of activated factors V and X.

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19.8 Blood Groups and Blood Types 687

enzyme. Among these substances are thrombin, activated factor XII, and itself, called a thrombus (THROM-bus), may dissolve spontaneously. If it
tissue plasminogen activator (t-PA), which is synthesized in endothelial remains intact, however, the thrombus may become dislodged and be
cells of most tissues and liberated into the blood. Once plasmin is formed, swept away in the blood. A blood clot, bubble of air, fat from broken
C
it can dissolve the clot by digesting fibrin threads and inactivating sub- bones, or a piece of debris transported by the bloodstream is called an
stances such as fibrinogen, prothrombin, and factors V and XII. embolus (EM-bō-lus; em- = in; -bolus = a mass). An embolus that breaks
Even though thrombin has a positive feedback effect on blood away from an arterial wall may lodge in a smaller-diameter artery down-
op
clotting, clot formation normally remains localized at the site of dam- stream and block blood flow to a vital organ. When an embolus lodges in
age. A clot does not extend beyond a wound site into the general cir- the lungs, the condition is called pulmonary embolism.
culation, in part because fibrin absorbs thrombin into the clot. An-
other reason for localized clot formation is that because of the disper- Checkpoint
sal of some of the clotting factors by the blood, their concentrations 18. What is hemostasis?
are not high enough to bring about widespread clotting.
19. How do vascular spasm and platelet plug formation occur?
yr
Several other mechanisms also control blood clotting. For example,
20. What is fibrinolysis? Why does blood rarely remain clotted inside
endothelial cells and white blood cells produce a prostaglandin called
- blood vessels?
prostacyclin (pros-ta-SI -klin) that opposes the actions of thromboxane
A2. Prostacyclin is a powerful inhibitor of platelet adhesion and release. 21. How do the extrinsic and intrinsic pathways of blood clotting differ?
In addition, substances that delay, suppress, or prevent blood clot- 22. Define each of the following terms: anticoagulant, thrombus,
ig
ting, called anticoagulants (an′-tī-kō-AG-ū-lants), are present in blood. embolus, and thrombolytic agent.
These include antithrombin, which blocks the action of several factors,
including XII, X, and II (prothrombin). Heparin, an anticoagulant that is
produced by mast cells and basophils, combines with antithrombin
19.8 Blood Groups and
ht
and increases its effectiveness in blocking thrombin. Another antico-
agulant, activated protein C (APC), inactivates the two major clotting
factors not blocked by antithrombin and enhances activity of plasmino-
Blood Types
gen activators. Babies that lack the ability to produce APC due to a ge-
netic mutation usually die of blood clots in infancy. OBJECTIVES

Intravascular Clotting
W
• Distinguish between the ABO and Rh blood groups.

Despite the anticoagulating and fibrinolytic mechanisms, blood clots • Explain why it is so important to match donor and recipient blood
sometimes form within the cardiovascular system. Such clots may be types before administering a transfusion.
initiated by roughened endothelial surfaces of a blood vessel resulting
ile
from atherosclerosis, trauma, or infection. These conditions induce
adhesion of platelets. Intravascular clots may also form when blood The surfaces of erythrocytes contain a genetically determined assort-
flows too slowly (stasis), allowing clotting factors to accumulate locally ment of antigens composed of glycoproteins and glycolipids. These
in high enough concentrations to initiate coagulation. Clotting in an antigens, called agglutinogens (a-gloo-TIN-ō-jens), occur in characteris-
unbroken blood vessel (usually a vein) is called thrombosis. The clot tic combinations. Based on the presence or absence of various anti-
gens, blood is categorized into different blood groups. Within a given
y,
blood group, there may be two or more different blood types. There
Clinical Connection
are at least 24 blood groups and more than 100 antigens that can be
detected on the surface of red blood cells. Here we discuss two major
Aspirin and Thrombolytic Agents blood groups—ABO and Rh. Other blood groups include the Lewis, Kell,
In patients with heart and blood vessel disease, the events of hemosta- Kidd, and Duffy systems. The incidence of ABO and Rh blood types var-
sis may occur even without external injury to a blood vessel. At low doses, ies among different population groups, as indicated in Table 19.5.
20
aspirin inhibits vasoconstriction and platelet aggregation by blocking syn-
thesis of thromboxane A2. It also reduces the chance of thrombus formation.
Due to these effects, aspirin reduces the risk of transient ischemic attacks TABL E 19.5 Blood Types in the United States
(TIA), strokes, myocardial infarction, and blockage of peripheral arteries.
BLOOD TYPE (PERCENTAGE)
Thrombolytic agents (throm′-bō-LIT-ik) are chemical substances that
are injected into the body to dissolve blood clots that have already formed to POPULATION GROUP O A B AB Rh+
restore circulation. They either directly or indirectly activate plasminogen.
20
European-American 45 40 11 4 85
The first thrombolytic agent, approved in 1982 for dissolving clots in the African-American 49 27 20 4 95
coronary arteries of the heart, was streptokinase, which is produced by
Korean-American 32 28 30 10 100
streptococcal bacteria. A genetically engineered version of human tissue
Japanese-American 31 38 21 10 100
plasminogen activator (tPA) is now used to treat victims of both heart
Chinese-American 42 27 25 6 100
attacks and brain attacks (strokes) that are caused by blood clots.
Native American 79 16 4 1 100

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688 CH A PT E R 19 The Cardiovascular System: The Blood

ABO Blood Group severe hemorrhage), or to improve immunity. However, the normal
components of one person’s RBC plasma membrane can trigger dam-
The ABO blood group is based on two glycolipid antigens called A aging antigen–antibody responses in a transfusion recipient. In an
C
and B (Figure 19.12). People whose RBCs display only antigen A have incompatible blood transfusion, antibodies in the recipient’s plasma
type A blood. Those who have only antigen B are type B. Individuals bind to the antigens on the donated RBCs, which causes agglutina-
-
who have both A and B antigens are type AB; those who have neither tion (a-gloo-ti-NA -shun), or clumping, of the RBCs. Agglutination is an
op
antigen A nor B are type O. antigen–antibody response in which RBCs become cross-linked to
Blood plasma usually contains antibodies called agglutinins (a- one another. (Note that agglutination is not the same as blood clot-
GLOO-ti-nins) that react with the A or B antigens if the two are mixed. ting.) When these antigen–antibody complexes form, they activate
These are the anti-A antibody, which reacts with antigen A, and the plasma proteins of the complement family (described in Section
anti-B antibody, which reacts with antigen B. The antibodies present 22.6). In essence, complement molecules make the plasma mem-
in each of the four blood types are shown in Figure 19.12. You do not brane of the donated RBCs leaky, causing hemolysis (hē-MOL-i-sis) or
yr
have antibodies that react with the antigens of your own RBCs, but rupture of the RBCs and the release of hemoglobin into the blood
you do have antibodies for any antigens that your RBCs lack. For ex- plasma. The liberated hemoglobin may cause kidney damage by clog-
ample, if your blood type is B, you have B antigens on your red blood ging the filtration membranes. Although quite rare, it is possible for
cells, and you have anti-A antibodies in your blood plasma. Although the viruses that cause AIDS and hepatitis B and C to be transmitted
agglutinins start to appear in the blood within a few months after through transfusion of contaminated blood products.
ig
birth, the reason for their presence is not clear. Perhaps they are Consider what happens if a person with type A blood receives a
formed in response to bacteria that normally inhabit the gastrointes- transfusion of type B blood. The recipient’s blood (type A) contains A
tinal tract. Because the antibodies are large IgM-type antibodies antigens on the red blood cells and anti-B antibodies in the plasma.
(see Table 22.3) that do not cross the placenta, ABO incompatibil- The donor’s blood (type B) contains B antigens and anti-A antibodies.
ht
ity between a mother and her fetus rarely causes problems. In this situation, two things can happen. First, the anti-B antibodies in
the recipient’s plasma can bind to the B antigens on the donor’s eryth-
Transfusions rocytes, causing agglutination and hemolysis of the red blood cells.
Second, the anti-A antibodies in the donor’s plasma can bind to the A
Despite the differences in RBC antigens reflected in the blood group antigens on the recipient’s red blood cells, a less serious reaction be-
systems, blood is the most easily shared of human tissues, saving cause the donor’s anti-A antibodies become so diluted in the recipi-
many thousands of lives every year through transfusions. A transfu- ent’s plasma that they do not cause significant agglutination and he-
W
-
sion (trans-FU-zhun) is the transfer of whole blood or blood compo- molysis of the recipient’s RBCs.
nents (red blood cells only or blood plasma only) into the bloodstream People with type AB blood do not have anti-A or anti-B antibodies
or directly into the red bone marrow. A transfusion is most often given in their blood plasma. They are sometimes called universal recipients
to alleviate anemia, to increase blood volume (for example, after a because theoretically they can receive blood from donors of all four
ile

FIGURE 19.12 Antigens and antibodies of the ABO blood types.

The antibodies in your plasma do not react with the antigens on your red blood cells.
y,
BLOOD TYPE TYPE A TYPE B TYPE AB TYPE O

A antigen B antigen Both A and B antigens Neither

A nor B antigen

Red blood cells

20

Plasma
20

Anti-B Anti-A Neither Both anti-A and

antibody antibody antibody anti-B antibodies

Q Which antibodies are usually present in type O blood?

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19.8 Blood Groups and Blood Types 689

TA B LE 1 9 . 6 Summary of ABO Blood Group Interactions Clinical Connection

BLOOD TYPE
C
Hemolytic Disease of the Newborn
CHARACTERISTIC A B AB O The most common problem with Rh incompatibility, hemolytic disease
Agglutinogen A B Both A Neither of the newborn (HDN), may arise during pregnancy (Figure 19.13). Nor-
op
(antigen) on RBCs and B A nor B mally, no direct contact occurs between maternal and fetal blood while a
woman is pregnant. However, if a small amount of Rh+ blood leaks from
Agglutinin (antibody) Anti-B Anti-A Neither Both anti-A
the fetus through the placenta into the bloodstream of an Rh− mother, the
in plasma anti-A nor and anti-B
anti-B mother will start to make anti-Rh antibodies. Because the greatest possi-
bility of fetal blood leakage into the maternal circulation occurs at delivery,
Compatible donor A, O B, O A, B, AB, O O the firstborn baby usually is not affected. If the mother becomes pregnant
blood types (no again, however, her anti-Rh antibodies can cross the placenta and enter
yr
hemolysis)
the bloodstream of the fetus. If the fetus is Rh−, there is no problem, be-
Incompatible donor B, AB A, AB — A, B, AB cause Rh− blood does not have the Rh antigen. If the fetus is Rh+, however,
blood types agglutination and hemolysis brought on by fetal–maternal incompatibility
(hemolysis) may occur in the fetal blood.
An injection of anti-Rh antibodies called anti-Rh gamma globulin
ig
(RhoGAM®) can be given to prevent HDN. Rh− women should receive
RhoGAM® before delivery, and soon after every delivery, miscarriage, or
abortion. These antibodies bind to and inactivate the fetal Rh antigens
blood types. They have no antibodies to attack antigens on donated
before the mother’s immune system can respond to the foreign antigens
RBCs. People with type O blood have neither A nor B antigens on their
by producing her own anti-Rh antibodies.
ht
RBCs and are sometimes called universal donors because theoreti-
cally they can donate blood to all four ABO blood types. Type O per-
sons requiring blood may receive only type O blood (Table 19.6). In FIGURE 19.13 Development of hemolytic disease of the newborn
practice, use of the terms universal recipient and universal donor is (HDN). (a) At birth, a small quantity of fetal blood usually leaks across
misleading and dangerous. Blood contains antigens and antibodies the placenta into the maternal bloodstream. A problem can arise when
other than those associated with the ABO system that can cause the mother is Rh− and the baby is Rh+, having inherited an allele for the
transfusion problems. Thus, blood should be carefully cross-matched Rh antigens from the father. (b) On exposure to Rh antigen, the mother’s
W
or screened before transfusion. In about 80% of the population, solu- immune system responds by making anti-Rh antibodies. (c) During a
ble antigens of the ABO type appear in saliva and other body fluids, in subsequent pregnancy, the maternal antibodies cross the placenta into the
fetal blood. If the second fetus is Rh+, the ensuing antigen–antibody reaction
which case blood type can be identified from a sample of saliva.
causes agglutination and hemolysis of fetal RBCs. The result is HDN.
ile

Rh Blood Group HDN occurs when maternal anti-Rh antibodies cross the placenta
and cause hemolysis of fetal RBCs.
The Rh blood group is so named because the Rh antigen, called Rh
factor, was first found in the blood of the Rhesus monkey. The alleles
of three genes may code for the Rh antigen. People whose RBCs have
Rh antigens are designated Rh+ (Rh positive); those who lack Rh anti-
y,
gens are designated Rh− (Rh negative). Table 19.5 shows the inci-
dence of Rh+ and Rh− in various populations. Normally, blood plasma Rh–
does not contain anti-Rh antibodies. If an Rh− person receives an Rh+ mother
blood transfusion, however, the immune system starts to make anti-
Rh antibodies that will remain in the blood. If a second transfusion of
20
Rh+ blood is given later, the previously formed anti-Rh antibodies will Placenta
cause agglutination and hemolysis of the RBCs in the donated blood, Anti-Rh
First antibodies Second
and a severe reaction may occur.
Rh+ Rh+
fetus fetus
Rh+
Typing and Cross-Matching Blood antigens
20
for Transfusion
(a) First (b) Between (c) Second
To avoid blood-type mismatches, laboratory technicians type the pregnancy pregnancies pregnancy
patient’s blood and then either cross-match it to potential donor blood
or screen it for the presence of antibodies. In the procedure for ABO Q Why is the firstborn baby unlikely to have HDN?
blood typing, single drops of blood are mixed with different antisera,

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690 CH A PT E R 19 The Cardiovascular System: The Blood

solutions that contain antibodies (Figure 19.14). One drop of blood is FIGURE 19.14 ABO blood typing. The boxed areas show
mixed with anti-A serum, which contains anti-A antibodies that will agglutination (clumping) of red blood cells.
agglutinate red blood cells that possess A antigens. Another drop is
C
mixed with anti-B serum, which contains anti-B antibodies that will In the procedure for ABO blood typing, blood is mixed with anti-A serum
agglutinate red blood cells that possess B antigens. If the red blood cells and anti-B serum.
agglutinate only when mixed with anti-A serum, the blood is type A. If
op
the red blood cells agglutinate only when mixed with anti-B serum, the Anti-A serum Anti-B serum
blood is type B. The blood is type AB if both drops agglutinate; if neither
drop agglutinates, the blood is type O.
In the procedure for determining Rh factor, a drop of blood is
mixed with antiserum containing antibodies that will agglutinate

Jean Claude Revy/Phototake

Jean Claude Revy/Phototake

RBCs displaying Rh antigens. If the blood agglutinates, it is Rh+; no
yr
agglutination indicates Rh−.
Once the patient’s blood type is known, donor blood of the same
ABO and Rh type is selected. In a cross-match, the possible donor
RBCs are mixed with the recipient’s serum. If agglutination does not
occur, the recipient does not have antibodies that will attack the do-
ig
nor RBCs. Alternatively, the recipient’s serum can be screened against Untreated blood Treated with Treated with Blood type
anti-A serum anti-B serum
a test panel of RBCs having antigens known to cause blood transfu-
sion reactions to detect any antibodies that may be present.
ht
Clinical Connection A

Anticoagulants
Patients who are at increased risk of forming blood clots may receive an-
ticoagulants. Examples are heparin or warfarin. Heparin is often adminis-
tered during hemodialysis and open-heart surgery. Warfarin (Coumadin®) B
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acts as an antagonist to vitamin K and thus blocks synthesis of four clot-
ting factors. Warfarin is slower acting than heparin. To prevent clotting in
donated blood, blood banks and laboratories often add substances that
remove Ca2+; examples are EDTA (ethylenediaminetetraacetic acid) and
CPD (citrate phosphate dextrose).
ile
AB

Checkpoint
23. What precautions must be taken before giving a blood transfusion?
y,
24. What is hemolysis, and how can it occur after a mismatched O
blood transfusion?
25. Explain the conditions that may cause hemolytic disease of the
Jean Claude Revy/Phototake
newborn.
Q What is agglutination?
20

Disorders: Homeostatic Imbalances red-colored hemoglobin circulating in skin blood vessels. Among the
most important causes and types of anemia are the following:
• Inadequate absorption of iron, excessive loss of iron, increased iron
requirement, or insufficient intake of iron causes iron-deficiency
Anemia
20
anemia, the most common type of anemia. Women are at greater
- risk for iron-deficiency anemia due to menstrual blood losses and
Anemia (a-NE-mē-a) is a condition in which the oxygen-carrying
capacity of blood is reduced. All of the many types of anemia are char- increased iron demands of the growing fetus during pregnancy.
acterized by reduced numbers of RBCs or a decreased amount of Gastrointestinal losses, such as those that occur with malignancy or
hemoglobin in the blood. The person feels fatigued and is intolerant ulceration, also contribute to this type of anemia.
of cold, both of which are related to lack of oxygen needed for ATP and • Inadequate intake of vitamin B12 or folic acid causes megaloblastic
heat production. Also, the skin appears pale, due to the low content of anemia, in which red bone marrow produces large, abnormal red

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Chapter Review 693

Chapter Review
C

Review 19.4 White Blood Cells

1. WBCs are nucleated cells. The two principal types are granulocytes (neu-
op
Introduction trophils, eosinophils, and basophils) and agranulocytes (lymphocytes and
1. The cardiovascular system consists of the blood, heart, and blood vessels. monocytes).
2. Blood is a liquid connective tissue that consists of cells and cell fragments 2. The general function of WBCs is to combat inflammation and infection. Neu-
surrounded by a liquid extracellular matrix (blood plasma). trophils and macrophages (which develop from monocytes) do so through
phagocytosis.
19.1 Functions and Properties of Blood
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3. Eosinophils combat the effects of histamine in allergic reactions, phago-
1. Blood transports oxygen, carbon dioxide, nutrients, wastes, and cytize antigen–antibody complexes, and combat parasitic worms. Basophils
hormones. liberate heparin, histamine, and serotonin in allergic reactions that intensify
the inflammatory response.
2. It helps regulate pH, body temperature, and water content of cells.
4. B lymphocytes, in response to the presence of foreign substances called
3. It provides protection through clotting and by combating toxins and
ig
antigens, differentiate into plasma cells that produce antibodies. Antibod-
microbes through certain phagocytic white blood cells or specialized blood
ies attach to the antigens and render them harmless. This antigen–antibody
plasma proteins.
response combats infection and provides immunity. T lymphocytes destroy
4. Physical characteristics of blood include a viscosity greater than that of wa- foreign invaders directly. Natural killer cells attack infectious microbes and
ter; a temperature of 38°C (100.4°F); and a pH of 7.35–7.45. tumor cells.
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5. Blood constitutes about 8% of body weight, and its volume is 4–6 liters in 5. Except for lymphocytes, which may live for years, WBCs usually live for only
adults. a few hours or a few days. Normal blood contains 5000–10,000 WBCs/μL.
6. Blood is about 55% blood plasma and 45% formed elements.
19.5 Platelets
7. The hematocrit is the percentage of total blood volume occupied by red
blood cells. 1. Platelets are disc-shaped cell fragments that splinter from megakaryocytes.
Normal blood contains 150,000–400,000 platelets/μL.
8. Blood plasma consists of 91.5% water and 8.5% solutes. Principal solutes
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2. Platelets help stop blood loss from damaged blood vessels by forming a
include proteins (albumins, globulins, fibrinogen), nutrients, vitamins, hor-
platelet plug.
mones, respiratory gases, electrolytes, and waste products.
9. The formed elements in blood include red blood cells (erythrocytes), white 19.6 Stem Cell Transplants from Bone Marrow
blood cells (leukocytes), and platelets.
and Cord Blood
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19.2 Formation of Blood Cells 1. Bone marrow transplants involve removal of red bone marrow as a source
1. Hemopoiesis is the formation of blood cells from hemopoietic stem cells in of stem cells from the iliac crest.
red bone marrow. 2. In a cord-blood transplant, stem cells from the placenta are removed from
the umbilical cord.
2. Myeloid stem cells form RBCs, platelets, granulocytes, and monocytes.
Lymphoid stem cells give rise to lymphocytes. 3. Cord-blood transplants have several advantages over bone marrow trans-
y,
plants.
3. Several hemopoietic growth factors stimulate differentiation and prolifera-
tion of the various blood cells. 19.7 Hemostasis
19.3 Red Blood Cells 1. Hemostasis refers to the stoppage of bleeding.

1. Mature RBCs are biconcave discs that lack nuclei and contain 2. It involves vascular spasm, platelet plug formation, and blood clotting
(coagulation).
20
hemoglobin.
2. The function of the hemoglobin in red blood cells is to transport oxygen and 3. In vascular spasm, the smooth muscle of a blood vessel wall contracts,
some carbon dioxide. which slows blood loss.
3. RBCs live about 120 days. A healthy male has about 5.4 million RBCs/μL of 4. Platelet plug formation involves the aggregation of platelets to stop
blood; a healthy female has about 4.8 million/μL. bleeding.
4. After phagocytosis of aged RBCs by macrophages, hemoglobin is 5. A clot is a network of insoluble protein fibers (fibrin) in which formed
20
recycled. elements of blood are trapped.
5. RBC formation, called erythropoiesis, occurs in adult red bone marrow of 6. The chemicals involved in clotting are known as clotting (coagulation)
certain bones. It is stimulated by hypoxia, which stimulates the release of factors.
erythropoietin by the kidneys. 7. Blood clotting involves a cascade of reactions that may be divided into
6. A reticulocyte count is a diagnostic test that indicates the rate of erythro- three stages: formation of prothrombinase, conversion of prothrombin into
poiesis. thrombin, and conversion of soluble fibrinogen into insoluble fibrin.

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694 CH A PT E R 19 The Cardiovascular System: The Blood

8. Clotting is initiated by the interplay of the extrinsic and intrinsic pathways 2. In the ABO blood group, the presence or absence of A and B antigens on the
of blood clotting. surface of RBCs determines blood type.
9. Normal coagulation requires vitamin K and is followed by clot retraction 3. In the Rh system, individuals whose RBCs have Rh antigens are classified as
C
(tightening of the clot) and ultimately fibrinolysis (dissolution of the clot). Rh+; those who lack the antigen are Rh−.
10. Clotting in an unbroken blood vessel is called thrombosis. A thrombus 4. Hemolytic disease of the newborn (HDN) can occur when an Rh− mother is
that moves from its site of origin is called an embolus. pregnant with an Rh+ fetus.
op
5. Before blood is transfused, a recipient’s blood is typed and then either
19.8 Blood Groups and Blood Types
cross-matched to potential donor blood or screened for the presence of
1. ABO and Rh blood groups are genetically determined and based on antibodies.
antigen–antibody responses.
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Critical Thinking Questions

ig
1. Shilpa has recently been on broad-spectrum antibiotics for a recurrent 3. Thomas has hepatitis, which is disrupting his liver functions. What kinds of
urinary bladder infection. While slicing vegetables, she cut herself and had symptoms would he be experiencing based on the role(s) of the liver related
difficulty stopping the bleeding. How could the antibiotics have played a role to blood?
in her bleeding?
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2. Mrs. Brown is in renal failure. Her recent blood tests indicated a hema-
tocrit of 22. Why is her hematocrit low? What can she be given to raise her
hematocrit?
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Answers to Figure Questions

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19.1 Blood volume is about 8% of your body mass, roughly 5–6 liters in males 19.9 Along with platelet plug formation, vascular spasm and blood clotting
and 4–5 liters in females. For instance, a 70-kg (150-lb) person has a blood contribute to hemostasis.
volume of 5.6 liters (70 kg × 8% × 1 liter/kg). 19.10 Serum is blood plasma minus the clotting proteins.
19.2 Platelets are cell fragments. 19.11 The outcome of the first stage of clotting is the formation of
19.3 Pluripotent stem cells develop from mesenchyme. prothrombinase.
19.4 One hemoglobin molecule can transport a maximum of four O2 mole- 19.12 Type O blood usually contains both anti-A and anti-B antibodies.
y,
cules, one O2 bound to each heme group. 19.13 Because the mother is most likely to start making anti-Rh antibodies
19.5 Transferrin is a plasma protein that transports iron in the blood. after the first baby is already born, that baby suffers no damage.
19.6 Once you moved to high altitude, your hematocrit would increase due to 19.14 Agglutination refers to clumping of red blood cells.
increased secretion of erythropoietin. 19.15 Some symptoms of sickle-cell disease are anemia, jaundice, bone pain,
19.7 Neutrophils, eosinophils, and basophils are called granular leukocytes shortness of breath, rapid heart rate, abdominal pain, fever, and fatigue.
20
because all have cytoplasmic granules that are visible through a light micro-
scope when stained.
19.8 Lymphocytes recirculate from blood to tissues and back to blood. After
leaving the blood, other WBCs remain in the tissues until they die.
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