Development of nonthrombogenicity of injured rabbit aortas despite inhibition of platelet adherence.
After removal of the endothelium from normal rabbit aortas or after injury to the neointima, the injured surfaces rapidly become nonreactive to circulating platelets. Experiments were done to determine whether prevention of the initial interaction of platelets with the surfaces would influence the loss of vessel wall reactivity. Inhibition of platelet accumulation on the subendothelium by the infusion of PGI2 (850 ng/kg/min) or the administration of dipyridamole (12.5 mg/kg initially followed by 5 mg/kg/hr) for periods of less than 8 hours inhibited platelet accumulation of platelets on the surfaces when the infusions were stopped. If the animals were treated for 8 hours, platelets did not accumulate on the surface when the drugs were discontinued. Thus, an injured vessel wall can develop a nonthrombogenic surface even when platelet adherence is prevented, although approximately 8 hours are required before the surface loses its ability to interact with platelets.
D000818:Animals; D001011:Aorta / Q000473:pathology*; D001792:Blood Platelets / Q000166:cytology* / Q000187:drug effects; D002448:Cell Adhesion; D004176:Dipyridamole / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D008297:Male; D008855:Microscopy, Electron, Scanning; D010974:Platelet Aggregation / Q000187:drug effects; D011817:Rabbits; D013917:Thrombin / Q000096:biosynthesis; D013997:Time Factors
D004176:Dipyridamole; D011464:Epoprostenol; D013917:Thrombin