Blood platelets do not provide endoperoxides for vascular prostacyclin production

Abstract

PROSTACYCLIN (PGI₂), the most active natural inhibitor of blood platelet aggregation described so far, is synthesised from the cyclic endoperoxide, PGH₂, derived from endogenous arachidonic acid by the cyclo-oxygenase enzyme system. Exogenous endoperoxides are also readily converted into PGI₂ (refs 1, 2). Indomethacin inhibits the cyclo-oxygenase activity and thereby prevents PGH₂ formation. Because of this lack of precursor, endogenous PGI₂ production of indomethacintreated tissue does not occur. However, when vascular tissue, pretreated with indomethacin, is incubated in platelet-rich plasma (PRP), its PGI₂ production is restored. On the basis of this observation it has been suggested that activated blood platelets can be a source of exogenous endoperoxides, stimulating the vascular prostacyclin formation and, consequently, limiting the growth of a platelet thrombus³. We now report results indicating that it is highly unlikely that blood platelets are able to promote vascular prostacyclin formation by supplying cyclic endoperoxides.