Endotoxin-induced platelet aggregation and secretion I. morphological changes and pharmacological effects

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Abstract
Endotoxin lipopolysaccharide (LPS) from Acinetobacter 199 A induced aggregation of blood platelets from immune adherence-positive species (rat, rabbit) but not from immune adherencenegative species such as pig and man. Aggregation occurred in 2 phases: the first was not accompanied by secretion of platelet constituents, was apparently a consequence of C3 activation, and was selectively inhibited by EGTA. The second phase of aggregation was associated with secretion of platelet granule contents, and with a lesser amount of cytoplasmic leakage. Secondary aggregation was abolished by the sulphydryl alkylating agent N-ethyl maleimide, and by agents which increased the level of cyclic AMP in platelets, such as prostaglandin Et (a stimulator of adenylate cyclase) and methyl xanthines (inhibitors of phosphodiesterase). Secondary aggregation was partly inhibited by agents which block platelet prostaglandin biosynthesis (e.g. aspirin, indomethacin). Primary aggregation was unaffected by these inhibitors at concentrations which blocked secondary aggregation.