This study examined the relation among platelet survival, thrombosis, and repeated vessel injury. With the use of 51Cr-labeled platelets, indwelling aortic catheters were shown to reduce platelet survival in rabbits and rats. In rabbits, thrombi were observed mainly at the aortic bifurcation and at the tip of the catheter. The amount of thrombus that formed in rabbits with short and long catheters was similar, but platelet survival was shortened only in rabbits with short and long catheters was similar, but platelet survival was shortened only in rabbits with long indwelling aortic catheters. In rats, the aortic catheters did not cause thrombosis, and platelet survival was shortened significantly in rats with both short and long catheters, but was more pronounced in animals with longer catheters. In both rabbits and rats, long aortic catheters caused more extensive vessel injury than the short catheters and this was associated with greater platelet interaction with the vessel wall. Platelet survival cannot be used as an estimate of thrombus formation, but may reflect the extent and frequency of vessel wall injury. thus, shortened platelet survival may represent increased platelet interaction with the damaged arterial wall and increased platelet consumption.

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Vessel injury, platelet adherence, and platelet survival.

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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.

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