Abstract
We have investigated the effects of PGE 1, 15-keto-PGE 1, 15-keto-13,14-dihydro-PGE 1 and 13,14-dihydro-PGE 1 on inhibition of human platelet aggregation by rat peritoneal neutrophils (RPN) and human polymorphonuclear neutrophils (PMN). Both RPN and PMN are known to synthesize nitric oxide (NO). In the presence of a threshold concentration of RPN or PMN the inhibitory effects of PGE 1 and 13,14-dihydro-PGE 1 on thrombin- or collagen-induced platelet aggregation were significantly increased as compared to the absence of cells, while 15-keto-PGE 1 and 15-keto-13,14-dihydro-PGE 1 were inactive. Oxyhemoglobin (oxy-Hb) abolished the synergistic effect of RPN and either PGE 1 or 13,14-dihydro-PGE 1 on thrombin-induced platelet aggregation, but under the experimental conditions used had much less effect on inhibition of collagen-induced aggregation. Potentiation of the antiaggregatory effect of PGE 1 and 13,14-dihydro-PGE 1 by NO might contribute to the therapeutic efficacy of exogenous PGE 1. This view is supported by the fact that plasma levels of PGE 1 and its active metabolite in patients receiving infusions of PGE 1 for treatment of peripheral arterial occlusive disease are in the order of magnitude acting synergistically with neutrophil-derived NO, while direct inhibition of platelet aggregation requires considerably higher concentrations of PGE 1 and 13,14-dihydro-PGE 1.
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