Reversal of aconitine-induced tachycardia by prostaglandins in the rabbit Langendorff preparation

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Abstract
The ability of PGA2, E1 E2, and F2α to alter: (a) the refractory period (as judged by the maximal driving frequency); (b) the rate of automatically beating aconitine-treated papillary muscles; and (c) the rate of both untreated and aconitine-treated Langendorff preparations, was studied. The addition of PGA2 (3.0 μmol), PGE2 (2.84 μmol), and PGF2α (2.1 μmol) to the perfusate returned heart rate to pre-aconitine levels in the Langendorff preparation, but this action was frequently accompanied by atrioventricular dissociation. In contrast, PGE1 (2.82 μmol) was ineffective in antagonising aconitine-induced tachycardia. In the normally beating rabbit Langendorff, PGF2α, (2.1 μmol) produced a slight but statistically significant negative chronotropic effect. Neither cardiac contractile force nor maximal driving frequency was altered by the addition of prostaglandins. These results suggest that PGA2, PGE2, and especially PGF2α may exert antiarrhythmic activity by direct action(s) upon in vitro rabbit myocardial preparations.

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