Page 312 - Anatomy and Physiology of Farm Animals, 8th Edition

Blood and Other Body Fluids / 297

Platelets and the Endothelium while nucleated endothelial cells can
VetBooks.ir When a vessel is injured and the endothe- synthesize additional cyclooxygenase.
This functional difference between the
lial cell lining is damaged so that the under-
lying connective tissue is exposed, platelets two cell types allows treatment with
aspirin to preferentially reduce throm-
adhere to collagen and other proteins in boxane synthesis by platelets. This is
the connective tissue. This platelet adhe­ the basis for the use of aspirin, at an
sion results from binding between platelet appropriate dose, when it is desirable
cell membrane proteins and the connec- to reduce the tendency for blood
tive tissue. The cell membrane of adhered coagulation.
platelets undergoes alterations, and secre- Some of the substances released by
tory granules are released. Platelets that aggregating platelets and some of the cell
have undergone these reactions are termed membrane components exposed by aggre-
activated platelets. The presence of acti- gated platelets act to promote coagulation.
vated platelets stimulates other platelets Thus, with larger sites of injury, more
to adhere to those already present. The platelets aggregate and more stimulants of
collection of platelets forms a platelet plug clotting are present in the local area.
that may be sufficient (together with local Coagulation is initiated when the local
vasoconstriction) to occlude an extremely concentration of these substances reaches
small opening in damaged vessels and some critical level. Platelets are required
bring about hemostasis. Platelet aggre­ for normal coagulation in response to vas-
gation is the term applied to the overall cular damage. Clotting may also be stimu-
sequence of events responsible for the lated outside of the body when a foreign
formation of the platelet plug. surface, such as the glass surface of a test
Platelet aggregation is also subject to reg- tube, induces the same platelet reactions as
ulation by two different eicosanoids: throm­ exposure to collagen.
boxane A (TXA ) and prostacyclin (PGI ).
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TXA is a stimulant of platelet aggregation,
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and prostacyclin inhibits platelet aggrega- Intrinsic and Extrinsic Coagulation
tion. When a vessel becomes damaged, the Pathways
activated platelets increase their synthesis
of TXA and are the primary source of The ultimate product of blood coagulation
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TXA , whereas the primary source of pros- is a relatively solid gel plug (clot or throm­
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tacyclin is intact, undamaged endothelial bus). This plug may be red or somewhat
cells. As the platelet plug grows and extends clear. The color varies with the number of
to areas where endothelial cells remain erythrocytes and other blood cells trapped
intact, the local concentration of prostacyc- in the clot. Erythrocytes and leukocytes
lin generated by undamaged endothelial are not necessary for coagulation, and they
cells acts to stop the growth of the platelet may or may not be present in a clot.
plug. TXA and serotonin (also released by A clot is relatively solid because of inter-
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adhered platelets) are both vasoconstrictors, lacing strands of fibrin (a protein polymer)
stimulating smooth muscle contraction to that are covalently crosslinked. Trapped
assist with hemostasis. within this network are other blood com-
Aspirin inhibits the formation of ponents (e.g., platelets, leukocytes, eryth-
eicosanoids by binding to and inhibiting rocytes), but the key element is the fibrin.
cyclooxygenase, an enzyme necessary Thus, the most basic explanation of coagu-
for their synthesis. TXA and prostacyc- lation is that it is a series of biochemical
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lin are both eicosanoids, so aspirin ini- reactions to produce and stabilize a protein
tially reduces the formation of both. polymer, fibrin.
However, platelets do not have nuclei The series or chain of biochemical reac-
and cannot synthesize new enzymes, tions that links initial exposure to collagen