OBJECTIVE:To investigate the effect of electroacupuncture (EA) at acupoints on the pericardium meridian on the expression of phosphorylated Akt (p-Akt) protein in rat myocardium after ischemia and reperfusion.METHODS:Seventy Wistar rats were evenly randomized into seven groups:the sham operation group (group A),ischemia-reperfusion model Ⅰ group (group B),ischemia-reperfusion model Ⅱ group (group C),EA at Neiguan (PC 6) group (group D),EA at Ximen (PC 4) group (group E),EA at Hegu (LI 4) group (group F),and LY294002 + EA at Neiguan (PC 6) group (group G).All processes were monitored by electrocardiography.In group A,the left anterior descending coronary artery was only threaded without ligation for 100 min.In group B,the left anterior descending coronary artery was ligated for 40 min and reperfused for 60 min.The left anterior descending coronary artery in group C was ligated for 40 min and reperfused for 100 min.Groups D,E,and F received EA for 20 min before undergoing ischemia for 40 min,and then received EA for 20 min before undergoing reperfusion for 60 min.Before modeling,group G was injected with LY294002 (0.3 mg/kg) into the tail vein,and then underwent the same intervention as the other EA groups.After reperfusion,myocardial tissue from the left cardiac ventricle was collected to enable West blot analysis of the p-Akt level,and analysis of electrocardiographic changes.RESULTS:In groups B and C,electrocardiography showed obvious elevation of the ST-segment Ⅱ lead (ECG-STⅡ),while the ECG-ST Ⅱ values were significantly lower in groups D,E,and G (P ＜ 0.01).The p-Akt levels in groups D and E were significantly greater than those in groups B and C (P ＜ 0.01).Compared with all other groups,group G showed a significantly different expression of p-Akt (P ＜ 0.01).CONCLUSION:The expression of p-Akt protein in cardiomyocytes was significantly greater in rats that were injected with LY294002 and received EA at Ximen (PC 4) compared with all other groups.This suggests that EA at Ximen (PC 4) resulted in activation of the phosphoinositide 3-kinase/Akt signaling pathway and phosphorylation of Akt.