Maes L, Andries R, Bourgain R H, Braquet P
Pharmacol Res Commun. 1986 Aug;18 Suppl:81-9. doi: 10.1016/0031-6989(86)90041-x.
Superfusion of PAF-acether over a branch of the mesenteric artery in the guinea pig invariably results in local endothelial injury and thrombus formation within 3-10 minutes. The thrombotic phenomena do not disappear when PAF-acether superfusion is discontinued, and even when forced embolization is induced. Within a very short interval renewal of thrombosis occurs at the same site. Several data point to a mechanism involving generation and release of endogenic PAF-acether. Recents findings on PAF-acether release by cultured endothelial cells indicate that in the in vivo situation this phenomenon could well be responsible for maintaining the thrombotic status as demonstrated by ultrastructural analysis. In a later stadium polymorphonuclear leukocytes are also involved in total thromboformation.
在豚鼠肠系膜动脉的一个分支上灌注血小板活化因子（PAF-乙酰醚），3 - 10分钟内总会导致局部内皮损伤和血栓形成。当停止PAF-乙酰醚灌注时，血栓形成现象不会消失，即使诱导强制栓塞时也是如此。在很短的时间间隔内，同一部位会再次发生血栓形成。一些数据表明存在一种涉及内源性PAF-乙酰醚生成和释放的机制。最近关于培养的内皮细胞释放PAF-乙酰醚的研究结果表明，在体内情况下，这种现象很可能如超微结构分析所示，是维持血栓形成状态的原因。在后期阶段，多形核白细胞也参与了整个血栓形成过程。
