Platelets as a source of vasoactive mediators.

Abstract

Human platelets release two major classes of vasoactive mediators during the secretion reaction: arachidonic acid metabolites and biogenic amines. All of these compounds, in particular thromboxane A2, PGF2 alpha, and serotonin (5-HT), are potent constrictors of human cerebral arteries in vitro. This contractile action of platelet-derived vasoconstrictors, as well as their prothrombotic activity, is antagonized by the vascular endothelium. Atherosclerotic alterations of the vessel wall endothelium, typical for cerebral ischemia and stroke, are associated with platelet hyperreactivity and enhanced mediator release during stimulation. Inhibition of platelet (hyper)function by acetylsalicylic acid or ticlopidine has clear protective effects in high-risk patients, underlining the significance of these platelet-derived products for cerebral thromboembolism and vasoconstriction. Whether more selective inhibitors of thromboxane generations or action are equally effective remains to be determined.