Post-Countershock Arrhythmias in Untreated and Digitalized Dogs

Recent studies suggest that countershock can stimulate cardiac autonomic nerves and that the resulting release of norepinephrine contributes to post-countershock (PCS) arrhythmias. β-Adrenergic receptor blocking agents, reserpine, cocaine, and cardiac-denervated preparations were used to evaluate this hypothesis in dogs under pentobarbital anesthesia. The suitability of the dog as an experimental system was examined. In the normal dog, the duration of PCS arrhythmia caused by a countershock of given energy was increased 100% by ouabain (0.05 mg/kg iv). In both normal dogs and dogs given ouabain (0.05 mg/kg iv), dichloroisoproterenol, pronethalol, and propranolol reduced the duration of PCS arrhythmia; reserpine, a norepinephrine depletor, reduced the duration of PCS arrhythmia; cocaine, a norepinephrine-uptake inhibitor possessing antiarrhythmic properties, increased the duration of PCS arrhythmia; denervation of the heart reduced the duration of PCS arrhythmia. Ouabain (0.05 mg/kg iv) reduced the duration of PCS arrhythmia in dogs with denervated hearts. These findings indicate that PCS arrhythmia in dogs is norepinephrine dependent. Evidence indicated that ouabain has an anti-adrenergic action on the heart also is presented.