A metabolite of sulphinpyrazone that is largely responsible for the effect of the drug on the platelet prostaglandin pathway.

I n view of the fairly large number of compounds that exhibit these differential effects it is necessary to review the relative importance of prostaglandin endoperoxides and thromboxane A 2 in platelet function. These results are consistent with prostaglandin endoperoxides being produced in large enough quantities when sodium arachidonate is added to a platelet suspension to cause aggregation themselves. This would explain why cyclo-oxygenase inhibitors inhibit platelet aggregation when it is induced in this way and why thromboxane synthetase inhibitors do not. Collagen is thought to activate the cleavage of arachidonate from platelet phospholipid. The precise quantities released are unknown. but the evidence points to the likelihood that the quantities are small and therefore must be converted into the more potent aggregating agent, thromboxane A,, before aggregation can be induced. Thus inhibitors of thromboxane synthetase are very potent inhibitors of collagen-induced aggregation. The reason for the lower potency of cyclooxygenase inhibitors on collagen-induced aggregation is not yet fully understood.