[Thrombogenic properties of the vessel and their inhibition].
Vascular thrombosis is the response to injury of blood and the vessel wall. Normal endothelium is a non thrombogenic surface and is transformed into a thrombogenic surface by endothelial injury, the first step in thrombosis and in the development of atherosclerosis and its thrombotic complications. Many agents may injure the endothelial cells leading to at least three types of lesions: endothelial desquamation, local increase in endothelial turnover without de-endothelialization, endothelial dysfunction. The study of the factors controlling the functions of normal endothelial cells, their proliferation and their pathological modifications is possible with the use of human endothelial cell culture. Local generation of thrombin increases the thrombogenicity of the subendothelium and the accumulation of platelets, an effect inhibited by heparin. Thrombin binds specifically to the endothelium, but in a conformation preventing platelet interaction. PGI2 production by the vessel wall is not the main factor preventing adhesion of platelets to the endothelium or the subendothelium. PGI2 limits thrombus formation at the injury site. In the event of stasis, the inhibition of PGI2 formation by aspirin increases the size of the thrombus containing platelets and fibrin. The thrombogenic response of the vessel wall varies according to the nature of endothelial injury: a lesion causing removal of the endothelium and followed by adhesion of a single layer of platelets; chronic or repeated injury giving rise to a platelet-fibrin thrombus. Initiation and development of the thrombogenic properties of the vessel wall can be inhibited by dietary manipulations or pharmacologic interventions acting at the level of the endothelium, the interactions of platelets and the vessel wall or the coagulation system.
D001241:Aspirin / Q000494:pharmacology; D001777:Blood Coagulation; D001792:Blood Platelets / Q000502:physiology; D001808:Blood Vessels / Q000187:drug effects / Q000293:injuries* / Q000503:physiopathology; D002478:Cells, Cultured; D004727:Endothelium / Q000378:metabolism / Q000503:physiopathology; D011464:Epoprostenol / Q000037:antagonists & inhibitors / Q000378:metabolism; D006801:Humans; D010973:Platelet Adhesiveness; D011485:Protein Binding; D013917:Thrombin / Q000378:metabolism; D013927:Thrombosis / Q000209:etiology
D011464:Epoprostenol; D013917:Thrombin; D001241:Aspirin
Propriétés thrombogéniques du vaisseau et leur inhibition.