目的 研究电针内关穴预处理对心肌缺血再灌注损伤(MIRI)家兔线粒体通透性转换孔(m PTP)开放的影响,及其心肌保护作用机制。方法 新西兰大耳白兔18只随机分为假手术组、模型组、电针组,每组6只。采用冠脉结扎法造模,电针内关组在造模前,给予电针刺激20 min/d,共5 d10采用黄嘌呤氧化酶法测定血清超氧化物歧化酶(SOD)活性,荧光技术测定心肌细胞线粒体膜电位变化,分光光度法测定520 nm处线粒体吸光度的变化反映线粒体m PTP的开放,原位末端标记法测细胞凋亡。结果与模型组比较,电针组心肌细胞SOD活力显著提高,凋亡指数降低(P〈0.01),线粒体膜电位显著提高(P〈0.05),线粒体吸光度明显降低(P〈0.01)。结论 电针内关穴可以有效改善心肌缺血再灌注损伤,对心肌产生保护作用。
Objective To investigate the cardioprotective mechanisms of electroacupuncture (EA) at Neiguan point on the opening of mPTP with in rabbits with myocardial isehemia-reperfusion injury (MIRI). Methods 18 New Zealand rabbits were randomly divided into the sham group, model group and EA group, 6 rats in each group. The models were established by ligating the coronary artery. The EA group was given electroacupuncture stimulation pretreatment 20 rain every day lasting for 5 days before establishing MIRI model. The serum SOD activity was determined by xanthine oxidase method; The mitochondrial membrane potential tested by fluorescent technique; The opening of mPTP in rats with MIRI was evaluated by determining the absorbance of mitochondrion 520 nm using speetrophotometrie method; The apoptosis was determined by TUNEL. Results Compared with the model group, the SOD activity of myocardial cell in the EA group was improved obviously, the apoptotic index was decreased (P〈0.01), the mitochondrial membrane potential was improved dramatically (P〈 0.05), the absorbance of mitoehondrion was reduced significantly (P〈0.01). Conclusion The EA at Neiguan point could improve the MIRI and showed cardioproteetive effects.