[5-阿片受体参与心脏和线粒体适应慢性持续缺氧后对缺血再灌注影响的抵抗力增强]。

E S Prokudina, L N Maslov, Yu V Bushov, M V Korobov, A A Podolskii, Sh Wang, Yu B Lishmanov
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引用次数: 0

摘要

研究了心脏Ϭ-opioid受体(OR)在慢性持续常压缺氧(CCNH)适应大鼠心脏和心肌线粒体对缺血再灌注的抵抗中所起的作用。大鼠在12% O2条件下连续CCNH 21天。诱发离体灌注心脏局部缺血(45分钟)和再灌注(30分钟)。对CCNH的适应促进了再灌注时坏死心肌细胞肌酸激酶释放的减少,并改善了心脏收缩力的再灌注恢复。适应大鼠线粒体呼吸和MPT孔状态对缺血再灌注的抵抗更强。用TIPP(0) (30 nM/l,选择性Ϭ-OR-antagonist)或硝三苯(1 nM/l,选择性52- or拮抗剂)灌注离体心脏完全消除CCNH的心脏保护作用。BNTX (1 nM/l,选择性Ϭ-OR-antagonist)对CCNH的心脏保护作用无影响。这些数据表明,心脏52-OR参与了大鼠适应CCNH后心脏和线粒体对缺血再灌注的抵抗力增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[INVOLVEMENT OF 5-OPIOID RECEPTORS IN THE INCREASED RESISTANCE OF HEART AND MITOCHONDRIA TO IMPACT OF ISCHEMIA-REPERFUSION AFTER ADAPTATION TO CHRONIC CONTINUOUS HYPOXIA].

It was investigated the involvement of cardiac Ϭ-opioid receptors (OR) in increasing the resistance of the heart and myocardial mitochondria to ischemia-reperfusion after adaptation rats to chronic continuous normobaric hypoxia (CCNH). Rats were subjected to CCNH for 21 days at 12 % O2. It was evoked global ischemia (45 minutes) and reperfusion (30 minutes) of the isolated perfused heart. Adaptation to CCNH promoted a reduction of creatine kinase release from necrotic cardiomyocytes during reperfusion and improved reperfusion recovery of heart contractility. Mitochondrial respiratory and state of MPT pore were more resistant to ischemia-reperfusion in adapting rats. Perfusion of isolated hearts with TIPP(0) (30 nM/l, a selective Ϭ-OR-antagonist) or naltriben (1 nM/l, a selective 52-OR-antagonist) completely eliminated the cardioprotective effect of CCNH. BNTX (1 nM/l, a selective Ϭ-OR-antagonist) had no effect on the cardioprotective effect of CCNH. This data suggest that cardiac 52-OR involved in the increased resistance of the heart and mitochondria to ischemia-reperfusion after adaptation rats to CCNH.

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