Abstract
The aim of this study was to find out whether, in neonatal rat cardiomyocytes, platelet-activating factor (PAF) can stimulate eicosanoid formation. For this purpose neonatal cardiomyocytes were incubated for 60 min at 37°C in HANKS buffer with PAF (10–1000 nM), and the eicosanoids thromboxane A 2 (TXA 2) and prostacyclin (PGI 2) were assessed in the supernatant as TXB 2 and 6-keto-PGF 1α, respectively, by an enzyme immunoassay. PAF caused concentration-dependent release of PGI 2; TXA 2, however, was significantly released only at the highest concentration of PAF (1000 nM). Acetylsalicylic acid (556 μM) and the PAF antagonist WEB 2086 (10 μM) significantly attenuated PAF-induced eicosanoid formation. We conclude that in neonatal rat cardiomyocytes PAF can induce eicosanoid formation and this effect is brought about by activation of a specific PAF receptor.
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