Endogenic PAF-acether production by guinea pig endothelial cells in experimental arterial thrombosis.
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.
D000818:Animals; D001792:Blood Platelets / Q000378:metabolism; D004727:Endothelium / Q000166:cytology / Q000378:metabolism / Q000648:ultrastructure; D006168:Guinea Pigs; D008297:Male; D009504:Neutrophils / Q000378:metabolism; D010972:Platelet Activating Factor / Q000096:biosynthesis*; D013927:Thrombosis / Q000378:metabolism*
D010972:Platelet Activating Factor