Inability of potassium canrenoate to convert experimentally induced ouabain arrhythmias in the canine heart.

The antiarrhythmic effects of potassium canrenoate were examined in 20 closedchest, pentobarbital-anesthetized dogs with ouabain-induced ventricular tachycardia. In a group of 8 dogs, a mean dose of ouabain of 64.4 ± 3.7 /ig/kg induced sustained ventricular tachycardia. Subsequent administration of potassium canrenoate (30 mg/kg, iv) caused ventricular fibrillation in 1 dog and sinus tachycardia in 3 dogs. Stimulation of the distal end of the cut right vagus in the latter 3 dogs slowed the sinus rhythm enough to permit the ventricular focus to become the dominant pacemaker. In the other 4 dogs, potassium canrenoate did not alter the ouabain-induced ventricular tachycardia. In a second group of 12 dogs, ventricular tachycardia was also induced by administering a toxic dose of ouabain (65.5 ± 2.9 /Ag/kg, iv). After ouabain intoxication, atrial overdrive suppression of the ventricular rhythm was initiated by electrically pacing the right atrium at a mean frequency of 184.5 ± 7.9 beats/min. Subsequent administration of potassium canrenoate (30 mg/kg, iv) to these dogs restored sinus rhythm in 4 of the dogs; however, stimulation of the distal end of the cut right vagus caused a reappearance of the ventricular ectopic focus. After potassium canrenoate administration, the minimum atrial pacing rate required to capture the ventricular rhythm was 160.9 ± 9.4 beats/min. This rate represents a significant reduction (P < 0.005) in the rate of the ouabain-induced ventricular ectopic focus, but in no instance was the focus directly suppressed by potassium canrenoate. Propranolol, in contrast to potassium canrenoate, restored normal sinus rhythm in all 20 ouabainintoxicated dogs and suppressed the ouabain-induced ectopic pacemaker during the period of vagally induced sinoatrial arrest. The results of this study show that potassium canrenoate fails to exert an antiarrhythmic effect against digitalis-induced arrhythmias and that any apparent restoration of sinus rhythm in response to potassium canrenoate is due to overdrive suppression of the ouabain-induced ventricular ectopic pacemaker.