Abstract
The platelet-activating factor (PAF) induced a marked increase of the thromboxane (TX) B 2-formation in the incubation medium of isolated myocardium and tissue from other organs. The content of the 6-oxo-prostaglandin (PG)F 1α, the inactive metabolite of PGI 2, remained uninfluenced or showed a small decrease. PAF, given in a concentration of 2.10 −9 mol/l or a single dose of 100 ng, significantly reduced the contraction force and the coronary flow of isolated guinea-pig hearts. This effect was connected with a high efflux of TXA 2. The PAF-antagonist, WEB 2086, nearly abolished the cardiac effects of PAF, and iloprost or a pretreatment with indomethacin markedly reduced the PAF-influence on the heart. The TXA 2-antagonist BM 13177 was ineffective. The results indicate a close interaction between the myocardial PAF-effect and the TXA 2-formation of the heart tissue, but gave no suggestion for a mediation of the PAF-effect by TXA 2. The PAF-antagonistic action of WEB 2086, iloprost and indomethacin could be of some interest in the therapy of cardiovasculatory diseases.
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