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
