Atherosclerosis. I. A leiomyoproliferative disease of the arteries resulting from breakdown of the endothelial barrier to potent blood growth factors. II. Perspectives in atheroprophylaxis.
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 understanding 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 endothelial 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.
D001161:Arteriosclerosis / Q000517:prevention & control*; D002118:Calcium / Q000494:pharmacology; D002395:Catecholamines / Q000378:metabolism; D015118:Eicosapentaenoic Acid / Q000494:pharmacology; D004727:Endothelium / Q000648:ultrastructure; D011464:Epoprostenol / Q000096:biosynthesis; D006487:Hemostasis; D006801:Humans; D009131:Muscle, Smooth, Vascular; D009135:Muscular Diseases / Q000209:etiology*; D010974:Platelet Aggregation; D011956:Receptors, Cell Surface / Q000502:physiology; D017479:Receptors, Platelet-Derived Growth Factor; D013312:Stress, Physiological / Q000150:complications / Q000378:metabolism; D013917:Thrombin / Q000502:physiology; D013921:Thrombocytopenia / Q000209:etiology
D002395:Catecholamines; D011956:Receptors, Cell Surface; D015118:Eicosapentaenoic Acid; D011464:Epoprostenol; D017479:Receptors, Platelet-Derived Growth Factor; D013917:Thrombin; D002118:Calcium