Abstract
For a historical survey of the pathogenesis of atherosclerosis the reader is referred to references 1 and 2.
Comprehension of the vessel-blood interface homeostasis hinges upon an un derstanding of the pathophysiology of angio-lymphoid relationships.
Even in the smooth contact of the intact hydrophobic intimal lining with the marginal flow of the circulatory stream, small amounts of thrombin and small aggregates of aging platelets float by under physiologic conditions. Since endo thelial cells of the vascular intima contain receptors for thrombin, filling these receptors with thrombin becomes a stimulus for the production of prostacyclin (PGI2) by the endothelial cells; PGI2 in turn inhibits adherence of the small platelet aggregates by ADP; homeostasis is maintained. The size of physiologic thrombin-producing platelet microaggregates is controlled by physiologic levels of antithrombin III.
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