Prog Clin Biol Res. 1989;301:315-9.

Prostaglandin H2 in human platelet activation: coactivator and substitute for thromboxane A2.

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Institute for Clinical Chemistry, Klinikum Mannheim, University of Heidelberg, FRG.

Abstract

(1) When platelets form TXA2 from endogeneous AA, PGH2 reaches concentrations very similar to those of TXA2 and high enough to produce strong platelet activation. Therefore, platelet activation by TXA2 appears to go along with an activation by PGH2. (2) PGH2 is a more potent stimulus of platelet shape change and aggregation than U 46619. (3) The agonism of PGH2 is limited by the formation of inhibitory prostaglandins, especially PGD2 at higher concentrations. That is why thromboxane synthase inhibitors in PRP and at a physiological HSA concentration do not augment platelet activation. (4) HSA promotes the formation of inhibitory PGD2 at the expense of agonistic PGH2.

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Prostaglandin H2 in human platelet activation: coactivator and substitute for thromboxane A2.

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