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通过氨基甲酸乙酯麻醉大鼠观察股神经电刺激对缺血- 再灌注心肌的影响,旨在证实外周神经刺激对心肌有无保护效应,并明确其可能的作用机制。心肌缺血区和梗塞区分别用伊文思蓝和氯化硝基四氮唑蓝染色确定,心肌梗塞范围定义为心肌梗塞区重量占心肌缺血区重量的百分比。所得结果如下:(1)在心肌缺血30 min 和再灌注120 min 过程中,梗塞心肌占缺血心肌的(54.96±0.82)%。 高频电刺激(10 V,100 Hz,1ms)股神经5 min 可使心肌梗塞范围减少到(36.94±1.34)% (P<0.01), 表明 (2)高频电刺激股神经对缺血-再灌注心肌有保护作用。然而,低频电刺激(10 V, 10 Hz, 1 ms)股神经对缺血-再灌注心肌梗塞范围无影响。 预先应用非选择性阿片肽受体阻断剂纳洛酮(5 mg/kg, i.v.)或非选择性KATP 通道阻断剂格列苯脲(5 mg/kg, i.v.)均能完全 (3)取消高频电刺激股神经对缺血-再灌注心肌的保护作用。以上结果提示,高频外周神经刺激可以减小缺血- 再灌注心肌的梗塞范围,其可能的作用机制是: 高频电刺激股神经时中枢神经系统内释放的内源性阿片肽和由此激活的心肌KATP通道的开放介导了这种保护作用。
The rats were anesthetized with urethane to observe the effects of electrical stimulation on the myocardial ischemia-reperfusion in order to confirm the protective effect of peripheral nerve stimulation on myocardium and to clarify its possible mechanism. Myocardial ischemic and infarct areas were determined by Evans blue and nitrochlorothiazide blue staining, respectively. Myocardial infarct size was defined as the percentage of myocardial infarct area weight to myocardial ischemic area weight. The results obtained are as follows: (1) During 30 min of myocardial ischemia and 120 min of reperfusion, myocardial infarction accounted for 54.96 ± 0.82% of ischemic myocardium. High frequency electrical stimulation (10 V, 100 Hz, 1 ms) for 5 min reduced the extent of myocardial infarction to (36.94 ± 1.34)% (P <0.01), indicating that (2) Reperfusion myocardial protection. However, low frequency electrical stimulation (10 V, 10 Hz, 1 ms) had no effect on the extent of ischemia-reperfusion myocardial infarction. Naloxone (5 mg / kg, iv), a non-selective opioid receptor blocker, or glibenclamide (5 mg / kg, iv), a nonselective KATP channel blocker, The protective effect of high frequency electrical stimulation on the ischemic - reperfused myocardium was abolished. The above results suggest that high-frequency peripheral nerve stimulation can reduce the infarct size of ischemic-reperfused myocardium, and its possible mechanism is that the endogenous opioid peptides released by the central nervous system during high-frequency electrical stimulation of the femoral nerve and thus The opening of the activated myocardium KATP channels mediates this protective effect.