Influence of anti-platelet drugs on platelet-vessel wall interactions.
The influence of in vitro treatment of platelets with antiplatelet drugs on the interaction of these cells with the subendothelium was studied using citrated human blood obtained from normal control donors. Reconstituted blood following drug treatment was circulated through a special chamber which housed everted segments of de-endothelialized rabbit aorta. The wall shear rate used in these studies was 800 sec-1. Surface coverage of platelets on the subendothelium were morphometrically evaluated. Aspirin, Ibuprofen, Prostaglandin E1 and 13-Azaprostanoic acid significantly reduced platelet thrombi on exposed subendothelium. The calcium antagonists, Quin 2 and Diltiazem, exerted similar inhibitory effects, whereas Verapamil was a poor inhibitor. Aspirin treatment significantly enhanced platelet adhesion to the exposed vascular surface. Salicylate and Salicylamide did not enhance platelet adherence. Only Aspirin enhanced the formation of lipoxygenase metabolites of radiolabeled arachidonate. Results suggest that drugs which inhibit platelet aggregation and secretion of granule contents reduce formation of platelet thrombi. However, these drugs may or may not have a similar influence on platelet interaction with the subendothelium leading to spreading, adherence or formation of aggregates.
Department of Laboratory Medicine and Pathology, University of Minnesota Health Sciences Center, University Hospitals and Clinics, Minneapolis 55455.
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D001241:Aspirin / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000166:cytology*; D006801:Humans; D066298:In Vitro Techniques; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D013927:Thrombosis / Q000517:prevention & control*; D013931:Thromboxanes / Q000096:biosynthesis
D002121:Calcium Channel Blockers; D010975:Platelet Aggregation Inhibitors; D013931:Thromboxanes; D001241:Aspirin