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18 recordsLinked to original sources
PubMed1976

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.

Ajmaline↗
PubMedDate not supplied

[Effect of Bunaftine on the aconitine-induced atrial arrhythmias in the dog].

Bunaftine has a quinidine-like vagolytic effect and does not act as a beta-blocking agent. Its effect on aconitine-induced atrial fibrillation in the dog was examined. It led to suproventricular tachycardia in all cases, but re-established the sinus rhythm in only 5/15. It is felt that this lack of success is attributable to the slowing of the frequency of the primary pacemaker on the part of the drug. Slowing down of atrioventricular and intraventricular conduction by Bunaftine was revealed by lengthening of the P-R interval and widening of the Q-RS complex. Decreased blood pressure following administration of the drug appears to be due to reduction of heart rate rather than altered myocardial inotropism or peripheral resistance.

Aconitine↗
PubMed1979

[Supraventricular tachyarrhythmias. Therapeutical efficiency of bunaftine administed in rapid bolus (author's transl)].

The authors exhibit the results obtained in 25 patients sumministring bunaftine in 3 mg/Kg in 1-2 min in rapid bolus i.v. By means a continuous ECG registration they could state that the antiarrhythmic effect is simultaneous with the distribution of the drug, obtaining the restoration of the sinus rhythm in about 90% of the patients. The Authors remark the lack of meaningful collateral effect by means a pre-treatment with diazepam-cortisone, according to their method.

Adult↗
PubMedDate not supplied

[Effect of Bunaftine on the ventricular tachycardia due to aconitine in the dog].

Suppression of aconitine-induced ventricular tachycardia in the dog with various doses of Bunaftine was attempted. Stable re-establishment of the sinus rhythm was achieved in only 3/15 cases, whereas in 3 tachicardia was unchanged, and in 9 fibrillation appeared, due, it is thought, to the effect of the drug on myocardial conductivity, since fibrillation was the most frequent outcome when high doses were used.

Aconitine↗
PubMed1976

[Medical treatment of arrhythmias in myocardial infarct. Results of the use of bunaftine].

After a short survey of the physiopathology of arrhythmia in myocardial infarction, especially at the initial stage, the results of using bunaphthine in 21 personal cases of myocardial infarction are reported and the fully satisfactory results described. This substance is held to be an effective, useful antiarrhythmia drug which can be usefully employed in the prophylaxis of arrhythmia in myocardial infarction.

Adult↗