Drug effects on platelet deposition after endothelial injury of the rabbit aorta.
Factors released from platelets deposited on injured endothelium have lately been increasingly implicated in the pathogenesis of atherosclerosis and neointimal hyperplasia. Inhibition of platelet activity has therefore been postulated to protect injured vessels from progressive degenerative disease. The objective of this study was to evaluate the effectiveness of platelet inhibiting drugs in decreasing the deposition of platelets after a standardized endothelial injury of the rabbit aorta. The aortic endothelium of 53 rabbits was denuded with a balloon catheter. Morphological changes were studied with light and electron microscopy in five rabbits. The influence of ibuprofen, acetylsalicylic acid, dipyridamole, verapamil, and prostacyclin upon the deposition of indium-111-labeled autogenous platelets 1 hr after injury was evaluated in 48 animals. The morphological studies demonstrated that platelets were deposited on the denuded aorta but no major platelet aggregation or thrombus formation occurred. The radionuclide studies showed that none of the drugs tested had any significant influence on the deposition of platelets. It is concluded that platelets immediately adhere to injured vessels but that the secondary platelet aggregation is minimal if the injury is limited to the endothelium. Conventional drugs mainly affecting platelet aggregation are ineffective in these circumstances.
D000818:Animals; D001011:Aorta / Q000293:injuries; D001161:Arteriosclerosis / Q000517:prevention & control*; D001241:Aspirin / Q000494:pharmacology; D004176:Dipyridamole / Q000494:pharmacology; D004727:Endothelium / Q000502:physiology*; D011464:Epoprostenol / Q000494:pharmacology; D007052:Ibuprofen / Q000494:pharmacology; D010973:Platelet Adhesiveness / Q000187:drug effects*; D011817:Rabbits; D014700:Verapamil / Q000494:pharmacology
D004176:Dipyridamole; D014700:Verapamil; D011464:Epoprostenol; D001241:Aspirin; D007052:Ibuprofen