电针内关穴对心肌缺血再灌注模型大鼠心肌梗死期间心律失常的影响

Effects of electroacupuncture at Neiguan(PC6)on arrhythmia during myocardial infarction in a rat model of myocardial ischemia-reperfusion

目的观察电针内关穴对大鼠心肌缺血再灌注急性期心律失常及心室缝隙连接蛋白43(Cx43)表达的影响。方法共选用40只Sprague-Dawley雄性大鼠。随机选取10只作为空白组,剩余的30只大鼠被随机分为模型组和电针组,每组15只。电针组大鼠于造模前接受双侧内关单次30 min电针干预;其余组不予干预但进行同样方法抓取和30 min的麻醉。使用PowerLab生理记录仪记录梗死30 min内心电图,实验结束后取大鼠的心肌组织与血清。采用苏木素-伊红(HE)染色观察各组大鼠心室梗死区心肌组织形态变化;采用免疫印迹法(WB)检测各组大鼠心肌组织中Cx43蛋白表达情况;酶联免疫吸附测定(ELISA)检测大鼠心肌组织Na^(+)-K^(+)-ATP酶活性和大鼠血清内源性类洋地黄因子(EDLF)含量。结果电针组与模型组大鼠心律失常分数无统计学差异,但电针组心律失常的总时长和平均每次心律失常的持续时间均减少(P<0.01)。HE染色结果显示,与空白组相比,模型组心肌细胞排列紊乱,损伤严重;电针组病理变化与模型组相似,但损伤程度相对较轻。WB结果显示,与空白组相比,模型组大鼠心肌组织Cx43的表达降低(P<0.01);与模型组相比,电针组大鼠Cx43表达升高(P<0.01);与空白组相比,模型组大鼠心肌组织Na^(+)-K^(+)-ATP酶活性显著下降(P<0.01);与模型组相比,电针组Na^(+)-K^(+)-ATP酶活性有所提高(P<0.01)。ELISA结果显示,与空白组相比,模型组大鼠血清EDLF含量显著提高(P<0.01);与模型组相比,电针组EDLF含量下降(P<0.01)。结论电针内关穴可延缓和减少心肌缺血再灌注大鼠心肌梗死期间心律失常的发作;其作用机制可能与调控心肌组织中Cx43的表达,改善大鼠心肌组织Na^(+)-K^(+)-ATP酶活性以及提高血清EDLF含量有关。

Objective To observe the effects of electroacupuncture(EA)at Neiguan(PC6)on arrhythmia during acute myocardial ischemia-reperfusion and the expression of connexin 43(Cx43)in rats.Methods A total of 40 Sprague-Dawley male rats were used.Ten rats were randomly selected as the blank group,and the remaining 30 rats were randomly divided into a model group and an EA group,with 15 rats in each group.Before modeling,rats in the EA group received one session of EA intervention at bilateral Neiguan(PC6)for 30 min;the other groups were treated with the same grasping and anesthesia for 30 min without intervention.PowerLab physiological recorder was used to record electrocardiograph within 30 min of infarction.After the experiment,cardiac tissue and serum were collected from rats.Hematoxylin-eosin(HE)staining was used to observe the morphological changes of myocardial tissue in the ventricular infarction area of rats in each group.The expression of Cx43 protein in the myocardium of each group was detected by Western blotting(WB).Enzyme-linked immunosorbent assay(ELISA)was used to determine the activity of Na^(+)-K^(+)-ATPase in myocardial tissue and the serum content of endogenous digitalis-like factor(EDLF)in rats.Results There was no statistical difference in arrhythmia score between the EA group and the model group,but the total duration and average duration of arrhythmia in the EA group were decreased(P<0.01).HE staining showed that compared with the blank group,myocardial cells in the model group were disorganized and seriously damaged.The pathological changes in the EA group were similar to those in the model group,but the damage was relatively minor.The results of WB showed that compared with the blank group,the Cx43 expression in myocardial tissue of the model group was decreased(P<0.01);compared with the model group,the Cx43 expression in the EA group was increased(P<0.01);compared with the blank group,the Na^(+)-K^(+)-ATPase activity in myocardial tissue of the model group was significantly decreased(P<0.01);compared with the model group,the Na^(+)-K^(+)-ATPase activity in the EA group was increased(P<0.01).ELISA results showed that compared with the blank group,the serum EDLF content in the model group was significantly increased(P<0.01);compared with the model group,the EDLF content in the EA group was decreased(P<0.01).Conclusion EA at Neiguan(PC6)can delay and reduce the onset of arrhythmia during myocardial infarction in the rat model of myocardial ischemia-reperfusion.Its mechanism of action may be related to the regulation of the Cx43 expression in myocardial tissue,improvement of the activity of Na^(+)-K^(+)-ATPase in myocardial tissue,and increase in the content of serum EDLF.