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Platelet-activating factor (PAF-acether, l-O-alkyl-2-acetyl-sn- glyceryl-phosphorylcholine) stimulates platelets independently from ADP release and formation of arachidonate (A) metabolites, is released from platelets by aggregating amounts of thrombin or collagen, and may account for physiopathologically relevant aggregations. PAF-acether induces reversible aspirin-resistant thrombocytopenia and bronchoconstriction (BC) when given iv at 60120 ng/kg to propranolol-treated guinea-pigs. BC is platelet- dependent, and is suppressed by prostacyclin or by platelet depletion. BC was reduced for 30-60 min by iv sulphynpyrazone (S, 100 mg/kg). Inhibition by S of A-induced BC and thrombocytopenia lasted 6 hrs. This agrees with the fact that S is metabolized to a more effective cyclooxygenase inhibitor. Surprisingly, S was inactive against thrombocytopenia by PAF-acether, suggesting that BC was not inhibited because of a primary platelet site of action of S. Nevertheless, when platelets were collected from S-treated animals, aggregation and the release reaction by PAF-acether were inhibited. Inhibition of aggregation was surmounted by increasing the amounts of PAF-acether, whereas the release reaction was still inhibited by 50 % when 35 times more PAF-acether were added. Aggregation by ADP was unaffected by S, whereas the time course of inhibition of A was as against BC. In vitro, S (0.1-1 mM) inhibited the release reaction by AA and by PAF-acether ; this was surmounted with high amounts of the latter, but not of the former : the mechanism of inhibition by S of PAF-acether and of A thus differs in vivo and in vitro and this may be relevant to its therapeutic effectiveness.

Interference Of Sulphynpyrazone With The Platelet And Bronchial Effects Of “Platelet-Activating Factor”