Mechanism of electroacupuncture at “Zusanli” (ST36) in improving cardiac function in mice with chronic heart failure

To observe the effect of electroacupuncture (EA) at “Zusanli” (ST36) on improving cardiac function in mice with chronic heart failure (CHF), so as to explore the mechanism of its regulation on the autonomic nervous system.

Eighteen C57BL/6J mice were randomly divided into sham-surgery, model, and EA groups, with 6 mice in each group. The model of myocardial ischemia followed by CHF was induced by ligation of the anterior descending branch of the left coronary artery. Two weeks after modeling surgery, EA intervention (0.5 mA, 2 Hz/15 Hz) was performed bilaterally at ST36 in the EA group, 20 min each time, once every other day for 4 weeks. The left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-systolic diameter (LVESD), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic diameter (LVEDD), and left ventricular end-diastolic volume (LVEDV) were evaluated using echocardiographic imaging. The exercise tolerance was observed in an exhaustive test. Electrocardiograms were recorded using an electrophysiological recording system to analyze heart rate (HR) changes before and after EA, and frequency domain analysis was used to analyze the heart rate variability (HRV), including low-frequency (LF) component, high-frequency (HF) component, and their ratio (LF/HF). Immunofluorescence was used to observe the number of choline acetyltransferase (ChAT)⁺/c-fos⁺ co-labeled neurons in the dorsal motor nucleus of the vagus (DMV).

In terms of cardiac function, compared with the sham-surgery group, the LVEF and LVFS were decreased (P＜0.001) and the LVESD, LVEDD, LVESV, and LVEDV were increased (P＜0.001, P＜0.01) two weeks after modeling of mice in the model group. After 2 weeks of EA intervention, the LVESD and LVESV in the EA group were significantly smaller than those in the model group (P＜0.05). After 4 weeks of intervention, the LVEF and LVFS in the EA group were significantly higher than those in the model group (P＜0.05), and the LVESD and LVESV were significantly reduced (P＜0.05, P＜0.01). Compared with the model group, EA significantly improved the exercise tolerance of CHF mice (P＜0.05). Compared with the sham-surgery group, the LF/HF in the model group and EA group were significantly increased (P＜0.05) 2 weeks after modeling, indicating autonomic imbalance. After 4 weeks of intervention, the LF/HF in the EA group showed lower trend than that in the model group but the difference was not statistically significant. Additionally, after immediate EA, HR decreased (P＜0.05, P＜0.01), HF increased (P＜0.01), and both LF and LF/HF decreased significantly (P＜0.05) of mice in the EA group, indicating that EA corrected the autonomic imbalance in CHF mice. The number of ChAT⁺/c-fos⁺ co-labeled neurons in the DMV of the EA group was significantly higher (P＜0.001) than that in the model group.

EA at ST36 significantly improved cardiac function and exercise tolerance in CHF mice. The underlying mechanism may be related to the activation of vagus efferent nerve and the regulation of autonomic nerve balance.