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.
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Unilever Research, Vlaardingen, The Netherlands
- G. HORNSTRA
- , E. HADDEMAN
- & J. A. DON
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