Gao Qin, Hu Jun-Feng, Yu Ying, Jiang Cui-Rong, Guan Su-Dong, Li Zheng-Hong
Department of Physiology, Bengbu Medical College, Bengbu 233030, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Jan;28(1):9-13.
To investigate whether the release of nitric oxide (NO) was involved in the cardioprotection of ethanol postconditioning in isolated rat hearts.
Hearts isolated from male SD rats were subjected to 30 min of regional ischemia (occlusion of left anterior descending artery) followed by 120 min of reperfusion. Ethanol postconditioning was fulfilled through perfusion of 50 mmol/L ethanol for 15 min (at the end of cardiac ischemia for 5 min and at the beginning of reperfusion for 10 min). The rats were divided into five groups: normal, ischemia and reperfusion, ethanol postconditioning, ethanol postconditioning + L-nitro-arginine-methylester (L-NAME) and ethanol postconditioning + atractyloside. The ventricular hemodynamic parameters and lactate dehydrogenase (LDH) release during reperfusion were measured. The infarct size was measured by TTC staining method and NO content was measured by nitric acid reductase method. The expressions of Bcl-2 and Bax mRNA were detected by RT-PCR analysis.
In contrast to ischemia and reperfusion, ethanol postconditioning improved left ventricular developed pressure, rate pressure product during reperfusion, reduced LDH release and infarct size. NO content was decreased. The ratio of Bcl-2/Bax was increased. Administration of nitric oxide synthase inhibitor L-NAME or mitochondrial permeability transition pore opener atractyloside both attenuated the role of ethanol postconditioning, which inhibited the recovery of hemodynamic parameters, the decreases of LDH and infarct size. NO content was decreased further. The ratio of Bcl-2/Bax was decreased.
The cardioprotection of ethanol postconditioning may be associated with reducing nitric oxide release, inhibiting the opening of mitochondrial permeability transition pore and decreasing the happening of apoptosis.
探讨一氧化氮（NO）释放是否参与乙醇后处理对离体大鼠心脏的心肌保护作用。
取雄性SD大鼠心脏，进行30分钟局部缺血（左前降支动脉阻断），随后再灌注120分钟。乙醇后处理通过灌注50 mmol/L乙醇15分钟来实现（在心脏缺血结束5分钟时及再灌注开始10分钟时）。大鼠分为五组：正常组、缺血再灌注组、乙醇后处理组、乙醇后处理+左旋硝基精氨酸甲酯（L-NAME）组和乙醇后处理+苍术苷组。测量再灌注期间的心室血流动力学参数和乳酸脱氢酶（LDH）释放。通过TTC染色法测量梗死面积，用硝酸还原酶法测量NO含量。通过RT-PCR分析检测Bcl-2和Bax mRNA的表达。
与缺血再灌注组相比，乙醇后处理改善了再灌注期间的左心室舒张末压、心率血压乘积，降低了LDH释放和梗死面积。NO含量降低。Bcl-2/Bax比值升高。给予一氧化氮合酶抑制剂L-NAME或线粒体通透性转换孔开放剂苍术苷均减弱了乙醇后处理的作用，抑制了血流动力学参数的恢复、LDH和梗死面积的减小。NO含量进一步降低。Bcl-2/Bax比值降低。
乙醇后处理的心肌保护作用可能与减少一氧化氮释放、抑制线粒体通透性转换孔开放及减少细胞凋亡的发生有关。
