Maruyama Y, Awaji T, Inoue M, Takeo S
Department of Pharmacology, Tokyo College of Pharmacy, Japan.
Arzneimittelforschung. 1991 Oct;41(10):1022-6.
The present study was undertaken to elucidate beta-adrenoceptor blocking effects of befunolol (BFE 60, CAS 39543-79-8) on changes in the myocardial metabolites induced by hypoxic respiration. When rats were subjected to hypoxic respiration, a significant increase in heart rate (about 13% increase) and a slight decline in mean aortic blood pressure (about 12% decrease) were observed at 1 min and 6 min after the onset of hypoxic respiration. The hypoxic respiration also elicited decreases in the myocardial ATP and creatine phosphate levels (each 18% decrease) and increases in the myocardial lactate (13% increase) and cyclic-AMP (20% increase) levels. In contrast, these changes were never observed throughout hypoxic respiration when rats had been treated with both reserpine and alpha-methyl-p-tyrosine methylester 20 to 22 h before experiment, suggesting that these metabolic alterations are mediated through beta-adrenoceptor stimulation. These hypoxic respiration-induced hemodynamic and metabolic changes were found to be suppressed by treatment with 1 and 10 micrograms/kg befunolol or 10 micrograms/kg propranolol to an appreciable degree. The results demonstrate protective action of befunolol, like propranolol, on hypoxia-induced changes in the myocardial energy metabolism.
本研究旨在阐明倍他洛尔（BFE 60，CAS 39543 - 79 - 8）对低氧呼吸诱导的心肌代谢物变化的β - 肾上腺素能受体阻断作用。当大鼠进行低氧呼吸时，在低氧呼吸开始后1分钟和6分钟时，观察到心率显著增加（约增加13%），平均主动脉血压略有下降（约下降12%）。低氧呼吸还引起心肌ATP和磷酸肌酸水平降低（各降低18%），以及心肌乳酸（增加13%）和环磷酸腺苷（增加20%）水平升高。相反，当大鼠在实验前20至22小时用利血平和α - 甲基 - 对 - 酪氨酸甲酯处理时，在整个低氧呼吸过程中均未观察到这些变化，这表明这些代谢改变是通过β - 肾上腺素能受体刺激介导的。发现用1和10微克/千克倍他洛尔或10微克/千克普萘洛尔处理可在相当程度上抑制这些低氧呼吸诱导的血流动力学和代谢变化。结果表明，倍他洛尔与普萘洛尔一样，对低氧诱导的心肌能量代谢变化具有保护作用。
