Antifibrillatory properties of the beta-adrenergic receptor antagonists, nadolol, sotalol, atenolol and propranolol, in the anesthetized dog.

The antifibrillatory and electrophysiologic actions of the beta-adrenergic receptor antagonists, d,l-sotalol, d,l-nadolol, d,l-atenolol and d,l-propranolol were examined in anesthetized dogs. All four drugs were equally effective in increasing the electrical threshold for induction of ventricular fibrillation, but efficacy failed to correlate with reported beta-blocking efficacy. The d-isomers of the respective beta-adrenergic receptor blocking agents, sotalol and propranolol, were equipotent and equally effective at increasing the fibrillation threshold compared to their respective racemates. The ability of beta-adrenergic antagonists to increase the fibrillation threshold could not be attributed to changes in intraventricular conduction, ventricular refractoriness, or ventricular excitability in common with all four drugs. The antifibrillatory actions of the beta-adrenergic receptor blocking drugs could not be attributed solely to either beta-adrenergic blockade or specific alterations in the membrane properties of the cardiac cell.