Metabolic effects of bunaftine, a new antiarrhythmic agent: comparison with quinidine, ajmaline, procainamide, xylocaine and propranolol.
The effects of bunaftine (Meregon), quinidine, ajmaline, procainamide, xylocaine and propranolol have been investigated on glycolysis and oxygen consumption of rabbit heart and on the metabolic rate of trained rats. Quinidine, bunaftine and ajmaline stimulated glycolysis, procainamide was inactive while xylocaine and propranolol inhibited it. Myocardial oxygen consumption was reduced by quinidine and bunaftine only at high concentrations. However quinidine at 1-10(5) g/ml showed stimulating effect. Ajmaline and procainamide were inactive; xylocaine had a weak stimulating effect at 1-10(-6), propranolol had a stimulating effect at 3-10(-5) and 1-10(6) while it had an inhibiting effect at 1-10(-4) and 5-10(-3). With the exception of xylocaine and propranolol, which inhibited metabolic rate of trained animals, all the other drugs were inactive. In view of these findings, the mechanism of action of anti-arrhythmic drugs is discussed and it is suggested that the metabolic changes they induce are to be considered as secondary or toxic effects, the main site of action being the myocardial cell membrane.
D000404:Ajmaline / Q000494:pharmacology; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001481:Basal Metabolism / Q000187:drug effects; D002082:Butylamines / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009281:Naphthalenes / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D011342:Procainamide / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011802:Quinidine / Q000494:pharmacology; D011817:Rabbits; D051381:Rats
D000889:Anti-Arrhythmia Agents; D002082:Butylamines; D009281:Naphthalenes; D000404:Ajmaline; D008012:Lidocaine; D011433:Propranolol; D011802:Quinidine; D011342:Procainamide