舒芬太尼后处理对大鼠心肌缺血再灌注时细胞凋亡的影响

Effect of sufentanil postconditioning on cardiomyocyte apoptosis during myocardial ischemia-reperfusion in rats

目的探讨舒芬太尼后处理对大鼠缺血再灌注时心肌细胞凋亡的影响。方法健康雄性SD大鼠36只，体重250～280g，采用随机数字表法，将大鼠随机分为3组（／t=12）：假手术组（s组）、缺血再灌注组（I／R组）和舒芬太尼后处理组（SP组）。采用结扎左冠状动脉30min，再灌注120min的方法制备心肌缺血再灌注模型。S组只挂线不结扎左冠状动脉；SP组于再灌注即刻静脉注射舒芬太尼3．0μg／kg。于缺血再灌注期间记录HR和MAP。于再灌注120rain时，处死大鼠，取心脏，测定心肌梗死面积，采用RT-PCR测定心肌BaxmRNA和Bcl-2mRNA的表达，采用TUNEL法检测心肌凋亡细胞，计算凋亡指数。结果三大鼠各时点HR比较差异无统计学意义（P〉0．05）；与S组比较，I／R组心肌缺血再灌注期间MAP降低（P〈0．05），SP组差异无统计学意义（P〉0．05），I／R组和SP组凋亡指数和BoxmRNA表达水平升高，I／R组Bcl-2mRNA表达水平降低，SP组Bcl-2mRNA表达水平升高（P〈0．05）；与I／R组比较，SP组心肌梗死面积、凋亡指数和BaxmRNA表达水平降低，Bcl-2mRNA表达水平升高（P〈0．05）。结论舒芬太尼后处理可能通过上调Bcl-2表达，下调Bax表达，抑制细胞凋亡，从而减轻大鼠心肌缺血再灌注损伤。

Objective To investigate the effect of sufentanil postconditioning on cardiomyocyte apoptosis during myocardial ischemia-reperfusion （I/R） in rats. Methods Thirty-six male Sprague-Dawley rats weighing 250-280 g were randomly divided into 3 groups （n = 12 each） ： sham operation group （group S）, I/R group and sufentanil postconditioning group （group SP）. Myocardial I/R was induced by occlusion of the left coronary artery for 30 min followed by 120 min reperfusion. Sufentanil 3.0μg/kg was injected iv at the beginning of reperfusion in group SP. HR and MAP were recorded during I/R. The rats were sacrificed at 120 min of reperfnsion and their he- arts were removed for determination of infarct size, number of apoptotic cardiomyocytes, and the expression of Bax mRNA and Bcl-2 mRNA, and apoptotic index was cacnlated. Results There was no significant difference in HR among the 3 groups （P 〉 0.05）. Compared with group S, MAP and Bcl-2 mRNA expression were significantly de- creased, apoptotic index and Bax mRNA expression increased in group I/R, and apoptotic index, and the expres- sion of Bax mRNA and Bcl-2 mRNA were increased in group SP （ P 〈 0.05）. Compared with group I/R, the in- farct size, apoptotic index and Bax mRNA expression were decreased, and Bcl-2 mRNA expression was increased in group SP （ P 〈 0.05 ）. Conclusion Sufentanil postconditioning can attenuate myocardial I/R injury in rats by up-regulating Bcl-2 expression, down-regulating Bax expression and inhibitting cardiomyocyte apoptosis.