Abstract
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.
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