ObjectiveTo observe the effects of pretreatment with electroacupuncture (EA) on neuron activity in the rostral ventrolateral medulla (RVLM) of rats with myocardial ischemia-reperfusion injury (MIRI) and explore the central regulatory mechanism of EA in attenuating MIRI.MethodsOf 72 SD rats, 12 were randomly allocated into the group of EA pretreatment + RVLM nucleus damage (EA + RVLM lesion group). The other 60 rats were randomized (20 rats each) into a sham-operation group, a model group, and an EA pretreatment group (EA group). Except for the rats in the sham-operation group, the models of MIRI were prepared by ligating the left anterior descending coronary artery in the model, EA, and EA + RVLM lesion groups. The rats of the EA group were intervened with EA at “Shénmén (神门HT7)” and “Tōnglĭ (通里HT5)”, 1 mA in current intensity and 2 Hz in frequency, for 20 min each time per day. Before modeling, the intervention was given for seven consecutive days. In the EA + RVLM lesion group, 3 weeks after microinjection with the neuronal apoptotic virus at bilateral RVLM, the same EA intervention as the EA group was provided. Afterward, the MIRI models were prepared. In the model group, no EA intervention was given. Using Powerlab electrophysiolograph, ST segment displacement value and arrhythmia score were recorded and analyzed before modeling, 30 min after ligation, and 120 min after reperfusion in each group. The concentration of cardiac troponin (cTnl) was detected with an ELISA assay kit. Using immunofluorescence staining, the expression level of c-fos protein of RVLM was detected in the sham-operation, model, and EA groups separately. Plexon multichannel acquisition processor was adopted to record the neuronal firing and field potential of RVLM in the sham-operation, model, and EA groups.ResultsST segment displacement value, arrhythmia score, and cTnl concentration 30 min after ligation and 120 min after reperfusion were all elevated in the model group compared to the sham-operation group (all P < 0
目的:观察电针预处理心经经穴对心肌缺血再灌注损伤(MIRI)大鼠小脑顶核(FN)神经元电活动的变化,探讨FN参与电针预处理对心肌的保护机制是否通过下丘脑外侧区(LHA)-FN神经通路实现。方法:将SD大鼠随机分为假手术组、模型组、电针组、损毁LHA+电针组,每组12只。记录各组大鼠Ⅱ导联心电图ST段位移值、检测血清中心肌肌钙蛋白Ⅰ(cTnⅠ)的含量;记录各组大鼠FN神经元放电并进行分析。结果:再灌注2 h ST段位移值及cTnⅠ含量分析结果可见,与假手术组比较,模型组显著升高(P<0.01);与模型组和损毁LHA+电针组比较,电针组显著降低(P<0.01,P<0.05)。各组大鼠FN神经元自相关分析可见各组均有中间神经元放电。与假手术组比较,模型组FN放电次数显著减少(P<0.01);与模型组和损毁LHA+电针组比较,电针组神经元放电次数显著增多(P<0.01,P<0.05),FN神经元放电次数与再灌注2 h ST段位移值、cTnⅠ含量存在显著负相关性(P<0.01)。结论:电针预处理心经经穴可提高大鼠FN中间神经元放电频率,减轻MIRI效应;损毁LHA后,电针预处理对MIRI大鼠的心肌保护效应降低,LHA-FN神经通路参与了针刺减轻MIRI的中枢整合机制。
