539
CHAPTER FOURTEEN
Blood
ent of plasma. In the presence of calcium ions, prothrombin
activator converts prothrombin into
thrombin
(factor IIa).
Thrombin, in turn, catalyzes a reaction that fragments F
brin-
ogen (factor I). The F brinogen fragments join, forming long
threads of F brin. ±ibrinogen is a soluble plasma protein, but
F
brin is insoluble. Thrombin also activates factor XIII, which
strengthens and stabilizes F
brin threads.
Once F brin threads form, they stick to exposed surfaces of
damaged blood vessels, creating a meshwork that entraps blood
cells and platelets. The resulting mass is a blood clot, which
may block a vascular break and prevent further blood loss.
The amount of prothrombin activator in the blood is
directly proportional to the degree of tissue damage. Once
a blood clot begins to form, it promotes additional clotting,
because thrombin also acts directly on blood clotting factors
other than F brinogen, causing prothrombin to form still more
thrombin. This type of self-initiating action is an example of a
positive feedback system,
in which the original action stim-
ulates more of the same type of action. Such a mechanism
produces unstable conditions and can operate for only a short
time in a living system, because life requires the maintenance
of a stable internal environment (see chapter 1, p. 9).
Normally, blood fl ow throughout the body prevents for-
mation of a massive clot in the cardiovascular system by
rapidly carrying excess thrombin away and keeping its concen-
tration too low to enhance further clotting. In addition, a sub-
stance called
antithrombin,
in the blood and on the surfaces
of endothelial cells that line blood vessels, limits thrombin
formation. Consequently, blood coagulation usually happens
only in blood that is standing still or moving slowly, and clot-
ting ceases where a clot contacts circulating blood.
one activating the next in a
cascade.
Coagulation may occur
extrinsically or intrinsically. Release of biochemicals from bro-
ken blood vessels or damaged tissues triggers the
extrinsic
clotting mechanism.
Blood contact with foreign surfaces in
the absence of tissue damage stimulates the
intrinsic clotting
mechanism.
The following sections describe these responses.
Blood coagulation is complex and uses many biochemi-
cals called
clotting factors.
They are designated by Roman
numerals indicating the order of their discovery. Vitamin K
is necessary for some clotting factors to function. Whether
the blood coagulates depends on the balance between fac-
tors that promote coagulation (procoagulants) and others
that inhibit it (anticoagulants). Normally, the anticoagulants
prevail, and the blood does not clot. However, as a result
of injury (trauma), biochemicals that favor coagulation may
increase in concentration, and the blood may coagulate.
The major event in blood clot formation is conversion
of the soluble plasma protein
F
brinogen
(factor I) into insol-
uble threads of the protein
F
brin
(f
g. 14.18)
. Activation of
certain plasma proteins by still other protein factors triggers
conversion of F
brinogen to F
brin.
Table 14.7
summarizes the
three primary hemostatic mechanisms: blood vessel spasm,
platelet plug formation, and blood coagulation.
Extrinsic Clotting Mechanism
The extrinsic clotting mechanism is triggered when blood con-
tacts damaged blood vessel walls or tissues outside blood ves-
sels. Such damaged tissues release a complex of substances
called
tissue thromboplastin
(factor III), that is associated with
disrupted cell membranes. Tissue thromboplastin activates fac-
tor VII, which combines with and activates factor X. ±urther,
factor X combines with and activates factor V. These reactions,
which also require calcium ions (factor IV), lead to production
and release of
prothrombin activator
by the platelets.
Prothrombin
(factor II) is an alpha globulin that the
liver continually produces and is thus a normal constitu-
TABLE
14.7
|
Hemostatic Mechanisms
Mechanism
Stimulus
Ef
ect
Blood vessel
spasm
Direct stimulus to vessel
wall or to pain receptors;
platelets release serotonin,
a vasoconstrictor
Smooth muscles in vessel
wall contract ref
exly;
vasoconstriction helps
maintain prolonged vessel
spasm
Platelet plug
Formation
Exposure oF platelets
to rough surFaces or to
collagen oF connective tissue
Platelets adhere to rough
surFaces and to each other,
Forming a plug
Blood
coagulation
Cellular damage and
blood contact with Foreign
surFaces activate Factors that
Favor coagulation
Blood clot Forms as a result
oF a series oF reactions,
terminating in the conversion
oF ±
brinogen into ±
brin
FIGURE 14.18
A scanning electron micrograph oF ±
brin threads
(2,800
×
).
In
disseminated intravascular clotting,
coagulation is abnormally acti-
vated in several regions oF the cardiovascular system. This condition
is usually associated with bacterial inFection or bacterial toxins in the
blood or with a disorder causing widespread tissue damage. Many
small clots Form and obstruct blood Flow into various tissues and
organs, particularly the kidneys. As plasma clotting Factors and plate-
lets are depleted, severe bleeding occurs.
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