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目的观察芬太尼对离体大鼠心肌缺血/再灌注损伤所致心肌细胞凋亡的影响并初步探讨其可能机制。方法选取2015年1月~2016年1月由哈尔滨医科大学动物中心提供的健康Wistar大鼠24只作为研究对象,随机分成正常对照组(C组)、缺血/再灌注损伤组(I/R组)和芬太尼组(F组),各8只。利用Langendorff离体灌流装置,复制大鼠心肌缺血/再灌注损伤模型。观察指标:冠脉流出液LDH活性、心肌组织匀浆SOD活性和MDA含量,电镜观察心肌超微结构等。结果芬太尼明显减少大鼠心肌缺血/再灌注后LDH的漏出,使SOD活性升高,MDA含量降低,心肌结构损伤减轻,同时使细胞凋亡减少。结论芬太尼能减轻大鼠心肌缺血/再灌注损伤,其机制与其具有抗氧化、清除自由基和抗凋亡的作用有关。
Objective To investigate the effect of fentanyl on cardiomyocyte apoptosis induced by myocardial ischemia / reperfusion injury in vitro and its possible mechanism. Methods Twenty - four healthy Wistar rats from January 2015 to January 2016 were randomly divided into normal control group (C group), ischemia / reperfusion injury group (I / R group Group) and fentanyl group (group F), each 8. Myocardial ischemia-reperfusion injury model was reproduced using Langendorff isolated perfusion device. Observed indicators: coronary effusion LDH activity, myocardial homogenate SOD activity and MDA content, electron microscopy myocardial ultrastructure. Results Fentanyl significantly reduced LDH leakage after myocardial ischemia / reperfusion in rats, increased SOD activity, reduced MDA content, reduced myocardial structural damage and decreased apoptosis. Conclusion Fentanyl can reduce the myocardial ischemia / reperfusion injury in rats, and its mechanism is related to its anti-oxidation, scavenging free radicals and anti-apoptotic effects.