[Mechanism of platelet aggregation and mode of action of platelet antiaggregants].
Platelets play an important role in arterial thrombosis. Following the adhesion of platelets to an injured vascular wall, platelet activation occurs, involving calcium fluxes, phosphoinositol metabolism, protein phosphorylation, arachidonate cascade. This leads to the formation of the fibrinogen membrane receptor, the IIb/IIIa glycoprotein complex. Platelet aggregation results from the binding of fibrinogen and other adhesive proteins to the IIb/IIIa complex between several platelets. Numerous drugs can interfere with platelet function. Among these, only aspirin and ticlopidine have been shown to be effective in controlled trials. Aspirin, by inhibiting cyclo-oxygenase, blocks thromboxane A2 formation. Ticlopidine, by inhibiting fibrinogen binding to the complex, is a potent antiaggregation agent.
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D001095:Arachidonic Acids / Q000378:metabolism; D001241:Aspirin / Q000494:pharmacology; D001808:Blood Vessels / Q000503:physiopathology; D000242:Cyclic AMP / Q000097:blood; D006801:Humans; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*
D001095:Arachidonic Acids; D010975:Platelet Aggregation Inhibitors; D000242:Cyclic AMP; D001241:Aspirin
Mécanisme de l'agrégation plaquettaire et mode d'action des antiagrégants plaquettaires.