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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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