Failure of potassium canrenoate to alter experimentally induced digitalis arrhythmias

Abstract

The antiarrhythmic effects of potassium canrenoate were examined under in vivo and in vitro conditions. In the pentobarbital anesthetized dog, ventricular tachycardia was produced by the i.v. administration of ouabain, 64.4 +/- 3.7 [mu]g/kg. Potassium canrenoate was administered in increments of 10 mg/kg until a total dose of 30 mg/kg had been achieved. 1 animal developed ventricular fibrillation and in the remaining 7 dogs, the ouabain-induced ectopic focus was not suppressed. However, in 3 dogs, a sinus or junctional tachycardia occured after potassium canrenoate was administered and the rates exceeded that of the ventricular focus. Stimulation of the distal right vagus, however, resulted in a suppression of the supraventricular rhythm and a reappearance of the ventricular ectopic focus. In the rabbit perfused isolated heart, potassium canrenoate (10-3 M) failed to prevent or reverse acetylstrophanthidin-induced arrhythmias. It is concluded that potassium canrenoate fails to suppress or reverse the cardiotoxic effects of digitalis in the intact dog heart or in isolated heart muscle preparations. In addition, sodium canrenoate does not prevent the positive inotropic action of ouabain.