Prevention of Abnormal Clotting
Clotting should
take place to stop bleeding, but too much clotting would obstruct vessels and
interfere with normal circulation of blood. Clots do not usually form in intact
vessels because the endothelium
(sim-ple squamous epithelial lining) is very smooth and repels the platelets
and clotting factors. If the lining becomes roughened, as happens with the
lipid depo-sits of atherosclerosis, a clot will form.
Heparin,
produced by basophils, is a natural antico-agulant that inhibits the clotting
process (although heparin is called a “blood thinner,” it does not “thin” or
dilute the blood in any way; rather it prevents a chemical reaction from taking
place). The liver pro-duces a globulin called antithrombin, which combines with and inactivates excess thrombin.
Excess thrombin would exert a positive feedback effect on the clotting cascade,
and result in the splitting of more prothrom-bin to thrombin, more clotting,
more thrombin formed, and so on. Antithrombin helps to prevent this, as does
the fibrin of the clot, which adsorbs excess thrombin and renders it inactive.
All of these factors are the external brake for this positive feedback
mech-anism. Together they usually limit the fibrin formed to what is needed to
create a useful clot but not an obstructive one.
Thrombosis
refers to clotting in an intact vessel; the clot itself is called a thrombus. Coronary throm-bosis, for
example, is abnormal clotting in a coronary artery, which will decrease the
blood (oxygen) supply to part of the heart muscle. An embolism is a clot or other tissue transported from elsewhere that
lodges in and obstructs a vessel.
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