The arrhythmogenic effect of platelet activating factor (PAF) is inhibited by PAF antagonist and by substances influencing eicosanoids

Platelet-activating factor (PAF) induced arrhythmogenic effects in ouabain-induced arrhythmias and in untreated guinea pigs. The ischemic induced arrhythmias are aggravated by PAF in open-chest dogs. TX receptor antagonizing substances such as BM 13177 and specific PAF antagonists for example BN 52021 and WEB 2086, completely inhibited the PAF induced cardiac arrhythmias. An inhibitor of lipoxygenase such as esculetin inhibited the PAF effect to a small extent, too. Non-specific PAF antagonists such as diltiazem, diazepam, buphenin and trapidil have no or only a slight influence on PAF induced arrhythmias, although the antiarrhythmic effect of diltiazem and trapidil was shown on ouabain induced arrhythmias without PAF. The present study supports the hypothesis that PAF aggravates cardiac arrhythmias under pathophysiological conditions in which PAF is involved. Specific PAF antagonists and TX receptor antagonists induce antiarrhythmic effects under these conditions.