Antiarrhythmic effects of bupuranolol against canine ventricular arrhythmias induced by halothane-adrenaline or two-stage coronary ligation

• Published in: Journal of cardiovascular pharmacology Vol. 1; no. 2; p. 205
• Main Authors: Hashimoto, K, Tsukada, T, Matsuda, H, Nakagawa, Y, Imai, S
• Format: Journal Article
• Language: English
• Published: United States 01.03.1979
• Subjects: Adrenergic beta-Antagonists - pharmacology; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac - chemically induced; Arrhythmias, Cardiac - drug therapy; Arrhythmias, Cardiac - etiology; Arrhythmias, Cardiac - physiopathology; Bupranolol - pharmacology; Coronary Vessels - physiology; Dogs; Electric Stimulation; Epinephrine - pharmacology; Halothane - pharmacology; Heart - drug effects; Ligation; Microelectrodes; Myocardial Contraction - drug effects; Propanolamines - pharmacology
• ISSN: 0160-2446
• DOI: 10.1097/00005344-197903000-00004

We compared the beta-adrenoceptor blocking actions of bupuranolol and propranolol using the response to isoprenaline of the strength of contraction of the canine blood-perfused ventricular muscle, of the rate and strength of contraction of the isolated guinea pig heart and of a guinea pig tracheal ring preparation. The potency ratios of bupuranolol to propranolol were 3.6, 3.0, 3.4, and 2.4, respectively. Bupuranolol decreased the maximum dV/dt of the canine ventricular action potential and had no sympathomimetic action. Bupuranolol effectively suppressed halothane-adrenaline ventricular arrhythmias in the dog, reflecting its potency as a beta-adrenoceptor antagonist. In contrast, bupuranolol did not suppress ventricular arrhythmias induced by two-stage coronary ligation in the dog. Compared to propranolol and certain other antiarrhythmic drugs, bupuranolol had weaker effects on prolonging the effective refractory period than on the maximum dV/dt of canine ventricular muscle. This suggests that lengthening of the refractory period may be important for suppressing the two-stage coronary ligation arrhythmia and that the mechanism of this arrhythmia might be reentry.