Thromboxane A2 biosynthesis during endotoxin-induced aggregation of platelets from normal and sensitized guinea-pigs.
Endotoxin lipopolysaccharides Escherichia coli O26:B6 and E. coli O127:B8 were weak inducers of aggregation in normal guinea-pig platelet-rich plasma (PRP), even in the presence of Ca2+. Indomethacin hardly inhibited endotoxin-induced aggregation, indicating that biosynthesis of thromboxane A2 (TXA2) was of little importance. In accordance with this conclusion TXA2 was not detectable by means of bioassay during endotoxin-induced aggregation in normal guinea-pig PRP. Pretreatment of the guinea-pigs with endotoxin sensitized their PRP to endotoxin. This was due to a humoral factor with a selectively directed towards the polysaccharide moiety of endotoxin. The combination of this factor with endotoxin indued a marked biosynthesis of TXA2 and concomitant platelet aggregation.
D000818:Animals; D001792:Blood Platelets / Q000378:metabolism; D004731:Endotoxins / Q000276:immunology*; D004926:Escherichia coli; D005260:Female; D006168:Guinea Pigs; D007114:Immunization; D010974:Platelet Aggregation; D011458:Prostaglandins E / Q000097:blood; D013928:Thromboxane A2 / Q000096:biosynthesis* / Q000097:blood / Q000502:physiology; D013931:Thromboxanes / Q000096:biosynthesis*
D004731:Endotoxins; D011458:Prostaglandins E; D013931:Thromboxanes; D013928:Thromboxane A2