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目的观察丙泊酚对2型糖尿病大鼠心肌缺血-再灌注损伤的影响。方法雄性Wister2型糖尿病模型大鼠21只,随机均分为三组:心肌缺血-再灌注组(DI组)、心肌缺血-再灌注+丙泊酚组(DP组)、假手术组(D组)。另取21只健康大鼠作为对照,随机均分为三组:心肌缺血-再灌注组(CI组)、心肌缺血-再灌注+丙泊酚组(CP组)、假手术组(C组)。DI组和CI组结扎冠状动脉左前降支30min后再灌注2h建立心肌缺血-再灌注模型;D组和C组只穿线不结扎;DP组和CP组在缺血前10min静脉泵注丙泊酚6mg·kg-1·h-1至再灌注结束。测定基础状态及再灌注2h末大鼠血清乳酸脱氢酶(LDH)、肌酸激酶(CK)、血清及心肌丙二醛(MDA)和超氧化物歧化酶(SOD)含量。结果与基础状态相比,再灌注2h末DI、DP、CI、CP组血清LDH和CK含量升高(P<0.05);与CI组相比,CP组血清LDH、CK、MDA含量降低(P<0.05),且血清和心肌SOD含量升高(P<0.05);与DI组相比,DP组心肌SOD含量升高(P<0.05)。结论丙泊酚减轻正常大鼠心肌缺血-再灌注损伤,但对2型糖尿病大鼠心肌缺血-再灌注损伤无明显保护作用。
Objective To observe the effect of propofol on myocardial ischemia reperfusion injury in type 2 diabetic rats. Methods Twenty - one male Wister2 diabetic rats were randomly divided into three groups: ischemia - reperfusion (DI) group, myocardial ischemia - reperfusion + propofol group (DP), sham operation group Group D). Another 21 healthy rats were randomly divided into three groups: myocardial ischemia-reperfusion group (CI group), myocardial ischemia-reperfusion + propofol group (CP group), sham operation group group). The model of myocardial ischemia-reperfusion was established by ligating the left anterior descending branch of coronary artery in DI group and CI group for 2 hours and then reperfusion for 2 hours. D group and C group were not ligated by thread only. Phenol 6mg · kg-1 · h-1 to the end of reperfusion. Serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), serum and myocardial malondialdehyde (MDA) and superoxide dismutase (SOD) were measured at baseline and at the end of 2h reperfusion. Results Compared with the basal state, the levels of serum LDH and CK in DI, DP, CI and CP groups were significantly increased at the end of 2h after reperfusion (P <0.05). Compared with CI group, the levels of serum LDH, CK and MDA in CP group were decreased <0.05), and the content of SOD in serum and myocardium increased (P <0.05). Compared with DI group, the content of SOD in DP group increased (P <0.05). Conclusion Propofol alleviates myocardial ischemia-reperfusion injury in normal rats, but has no protective effect on myocardial ischemia-reperfusion injury in type 2 diabetic rats.