Abstract: OBJECTIVE  To observe the effect of cyclic mechanical compression of Neiguan (PC 6) on myocardial infarct size and cardiac function in rats with myocardial ischemia, and to preliminarily investigate the possible mechanism by which this factor produces cardioprotective effects.METHODS  A total of 18 adult male SD rats were randomly divided into sham, model, and mechanical stimuli group, 6 rats in each group. The myocardial ischemia model was established by ligating the left anterior descending (LAD) branch of the coronary artery in the model and mechanical stimuli group, while threading but not ligating at LAD was applied in the sham group. In the mechanical stimuli group, the Neiguan (PC 6) was pressed by the self-made instrument, with a contact surface of 3 mm diameter circular silica gel head and a force of 150 g, and the pressing mode was 5 min of pressing and 5 min of relaxation, with 3 cycles as one group, with intervention once a day for 3 consecutive days. The TTC staining was used to measure myocardial infarction area. Left ventricular ejection fraction(LVEF)was measured by echocardiography. The myocardial expression of IL-1β, IL-6 and TNF-α were detected by Western blot. Serum adenosine concentration was detected by ELISA. The expression level of adenosine deaminase(ADA)in acupoints was detected by immunohistochemistry.RESULTS  Compared with sham group, myocardial infarction area of model group increased(P < 0.001), LVEF value decreased(P < 0.001), and there was no difference in serum adenosine content and ADA expression in acupoint area (P>0.05). Compared with model group, the myocardial infarction area and myocardial expression of IL-1β, IL-6 and TNF-α in mechanical stimuli group decreased (P < 0.01), LVEF value increased (P < 0.001), serum adenosine content increased (P < 0.01), and the expression level of adenosine deaminase in acupoints decreased (P < 0.05).CONCLUSION  Cyclic mechanical compression of Neiguan (PC 6) can reduce the infarct size and improve cardiac function in Myocardial ischemic rats. The mechanism may be related to mechanical stimuli limiting adenosine degradation by inhibiting the expression of ADA in acupoint, contributing to cardioprotection via increased adenosine concentration in the artery.