Tanonaka K, Matsumoto M, Miyake K, Minematsu R, Takeo S
Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuyama University, Japan.
Eur J Pharmacol. 1989 Jun 8;165(1):97-106. doi: 10.1016/0014-2999(89)90774-7.
The present study was designed to determine whether the 1-form of YM-12617, which was developed recently as an alpha 1-adrenoceptor blocker, is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism. Isolated rabbit hearts were perfused for 25 min under hypoxic conditions in the absence or the presence of 28 microM YM-12617, followed by 45 min with oxygenated perfusion medium, and functional and metabolic changes of the heart were examined. Hypoxia induced several pathophysiological changes. Upon subsequent reoxygenation, there was less than 10% recovery of the contractile force and an approximately 40% recovery of the myocardial high-energy phosphates. Treatment with YM-12617 during the hypoxic periods resulted in approximately 90% recovery of the cardiac contractile function upon subsequent reoxygenation. Treatment with YM-12617 restored the myocardial high-energy phosphates, such as ATP and creatine phosphate, to approximately 90 and 80% of the initial value, respectively, during the subsequent reoxygenation. These results suggest that YM-12617 is capable of protecting the myocardium from hypoxia-induced disturbances of cardiac function and metabolism.
本研究旨在确定最近开发的α1肾上腺素能受体阻滞剂YM-12617的1型是否能够保护心肌免受缺氧引起的心脏功能和代谢紊乱。在缺氧条件下，将离体兔心在不存在或存在28μM YM-12617的情况下灌注25分钟，然后用含氧灌注培养基灌注45分钟，并检查心脏的功能和代谢变化。缺氧诱导了几种病理生理变化。随后再给氧时，收缩力恢复不到10%，心肌高能磷酸盐恢复约40%。在缺氧期间用YM-12617治疗导致随后再给氧时心脏收缩功能恢复约90%。在随后的再给氧期间，用YM-12617治疗可使心肌高能磷酸盐如ATP和磷酸肌酸分别恢复到初始值的约90%和80%。这些结果表明，YM-12617能够保护心肌免受缺氧引起的心脏功能和代谢紊乱。
