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Arch Int Pharmacodyn Ther. 1994 Jan-Feb;327(1):40-55.

Bopindolol and its metabolite 18-502 attenuate regional myocardial acidosis during partial occlusion of the coronary artery in dogs.

Archives internationales de pharmacodynamie et de therapie

Y Abiko, H Gotoh, T Yokoyama, T Abiko, H Hashizume, K Akiyama

Affiliations

  1. Department of Pharmacology, Asahikawa Medical College, Japan.

PMID: 7944827

Abstract

The effects of bopindolol (a new, nonselective beta-adrenoceptor antagonist) and its active metabolite, 18-502, on the regional myocardial pH during coronary occlusion were studied. Mongrel dogs were anesthetized with pentobarbital and the thorax was opened to expose the heart. The left anterior descending coronary artery (LAD) was incompletely (or partially) occluded so that the LAD flow could be reduced to about one third of the original flow. Regional myocardial pH of the LAD area was continuously measured by a tissue pH monitor. Drugs were injected intravenously 30 minutes after LAD partial occlusion. The myocardial pH in the LAD area decreased in response to LAD partial occlusion (from 7.3-7.4 to 6.72-6.92), and the low pH value was sustained for 60 minutes after LAD occlusion. Atenolol (1 mg/kg) decreased heart rate markedly and attenuated the regional myocardial acidosis induced by LAD partial occlusion. Bopindolol (1 mg/kg) decreased heart rate and 18-502 (0.5 mg/kg) decreased heart rate and blood pressure. Both drugs attenuated to a similar degree the decrease of regional myocardial pH induced by LAD occlusion. In the dog whose heart rate was maintained constant, however, bopindolol (1 mg/kg) did not attenuate the decrease of regional myocardial pH induced by LAD occlusion. These results suggest that both bopindolol and 18-502 attenuate the ischemia-induced regional acidosis of the myocardium as does atenolol, and, hence, have an anti-ischemic action. The beneficial action of bopindolol on ischemia-induced myocardial acidosis is possibly due to a decrease of heart rate, which corresponds to a saving of energy in the myocardial cells.

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