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目的:评价神经病理性痛因素对大鼠心肌缺血再灌注损伤的影响。方法:清洁级健康雄性SD大鼠36只，10周龄，体重225～275 g，按随机数字表法分为3组(n n＝12)：对照组(C组)、心肌缺血再灌注组(IR组)和神经病理性痛＋心肌缺血再灌注组(NP＋IR组)。采用坐骨神经缩窄性损伤(CCI)法制备大鼠神经病理痛模型。于CCI前和CCI后3、7、14 d时测定机械缩足反应阈(MWT)和热缩足潜伏期(TWL)。于CCI后14 d时，采用结扎左冠状动脉30 min再灌注2 h的方法，建立心肌缺血再灌注损伤模型。于缺血前、缺血30 min、再灌注2 h时记录HR、MAP和心率血压乘积(RPP)。再灌注结束时，计算心肌梗死体积，采用Western blot法测定心肌Bcl-2、Bax和caspase-3表达水平。n 结果:与C组或IR组比较，NP＋IR组CCI后MWT降低，TWL缩短(n P<0.01)。与C组比较，IR组缺血再灌注时MAP、HR及RPP降低，心肌梗死体积增加，Bax和caspase-3表达上调，Bcl-2表达下调(n P<0.05或0.01)；与IR组比较，NP＋IR组心肌梗死体积减小，Bax和caspase-3表达下调，Bcl-2表达上调(n P0.05)。n 结论:神经病理性痛可减轻大鼠心肌缺血再灌注损伤，机制可能与抑制心肌细胞凋亡有关。“,”Objective:To evaluate the effects of neuropathic pain (NP) factors on myocardial ischemia-reperfusion (I/R) injury in rats.Methods:Thirty-six clean-grade male Sprague-Dawley rats, aged 10 weeks, weighing 225-275 g, were divided into 3 groups (n n=12 each) using a random number table method: control group (group C), myocardial I/R group (group IR), and NP plus myocardial I/R group (group NP+ IR). The NP model was established by chronic constriction injury (CCI) to the sciatic nerve in anesthetized rats.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before CCI and at 3, 7 and 14 days after CCI.At 14 days after CCI, myocardial I/R injury was established by ligating the left coronary artery for 30 min followed by 2-h reperfusion.Heart rate (HR), mean arterial pressure (MAP) and the product of heart rate and blood pressure (RPP) were recorded before ischemia, at 30 min of ischemia, and at 2 h of reperfusion.The myocardial infarct size was calculated at the end of reperfusion.The expression of Bcl-2, Bax and casepase-3 in myocardial tissues was detected by Western blot.n Results:Compared with group C or group IR, the MWT was significantly decreased, and TWL was shortened after CCI in group NP + IR (n P<0.01). Compared with group C, MAP, HR and RPP were significantly decreased during I/R, myocardial infarct size was increased, the expression of Bax and caspase-3 was up-regulated, the expression of Bcl-2 was down-regulated in group IR (n P<0.05 or 0.01). Compared with group IR, myocardial infarct size was significantly reduced, the expression of Bax and casepase-3 was down-regulated, Bcl-2 expression was up-regulated, and no significant change was found in MAP, HR and RPP in group NP+ IR (n P<0.05).n Conclusion:NP can reduce myocardial I/R injury in rats, and the mechanism may be related to inhibiting apoptosis in cardiomyocytes.