Groves H M, Kinlough-Rathbone R L, Mustard J F
Arteriosclerosis. 1986 Mar-Apr;6(2):189-95. doi: 10.1161/01.atv.6.2.189.
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.
从正常兔主动脉去除内皮后或新内膜损伤后，损伤表面对循环血小板迅速失去反应性。进行实验以确定防止血小板与表面的初始相互作用是否会影响血管壁反应性的丧失。通过输注前列环素（PGI2，850 ng/kg/分钟）或给予双嘧达莫（初始剂量12.5 mg/kg，随后5 mg/kg/小时），持续时间少于8小时，抑制血小板在基底膜下的聚集，当输注停止时，可抑制血小板在表面的聚集。如果动物接受治疗8小时，停药后血小板不会在表面聚集。因此，即使防止血小板黏附，受损的血管壁仍可形成非血栓形成表面，尽管表面失去与血小板相互作用的能力大约需要8小时。
