Cardioprotective effects of hydrolyzed bopindolol against contractile dysfunction produced by coronary stenosis and reperfusion in dogs
Autor: | K, Noguchi, Y, Aniya, Y, Ojiri, T, Chibana, T, Matsuzaki, N, Shiroma, K F, Fong, M, Uza, M, Sakanashi |
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Rok vydání: | 1994 |
Předmět: |
Male
Hydrolysis Myocardium Adrenergic beta-Antagonists Blood Pressure Coronary Disease Heart Myocardial Reperfusion Injury In Vitro Techniques Myocardial Contraction Propranolol Rats Rats Sprague-Dawley Disease Models Animal Electrocardiography Dogs Heart Rate Coronary Circulation Pindolol Injections Intravenous Lactates Animals Female Lactic Acid Lipid Peroxidation |
Zdroj: | Archives internationales de pharmacodynamie et de therapie. 327(3) |
ISSN: | 0003-9780 |
Popis: | The effects of the active metabolite (18-502) of bopindolol, which is a new nonselective beta-adrenoceptor antagonist, were studied on the ischemic changes in myocardial segment shortening, cardiac lactate metabolism and S-T segment of subendocardial electrocardiogram during coronary stenosis and on their recoveries after reperfusion in anesthetized dogs, and were compared with those of propranolol at a dose exhibiting a comparable degree of beta 1-blocking activity. In the presence of coronary stenosis, intravenous administration of 18-502 (5 micrograms/kg) and propranolol (0.2 mg/kg), but not saline, produced significant improvements of regional myocardial dysfunction, lactate production and S-T segment elevations in the ischemic myocardium, which were associated with significant decreases in heart rate and cardiac contractility. After release of the stenosis, administration of 18-502, but not propranolol, resulted in a significantly accelerated recovery of the ischemic segment function as compared with the control group. In rat heart homogenates, 18-502 inhibited the lipid peroxidation approximately 4 times more potently than propranolol. These data show that 18-502 exerts favorable effects during myocardial ischemia produced by coronary stenosis and that it has a cardioprotective action against the contractile dysfunction following reperfusion. |
Databáze: | OpenAIRE |
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