健心平律丸对心律失常和水通道蛋白4的影响

Effect of Jian-xin-ping-lu pellet on arrhythmia and expression of aquaporin 4 following myocardial ischemia-reperfusion injury of rats

目的 :探讨健心平律丸对各类心律失常的作用及其对大鼠心肌缺血再灌注心律失常和水通道蛋白 4的作用。方法 :将 180例各种心律失常患者随机分为健心平律丸治疗组 (治疗组 110例 )和胺碘酮治疗组 (对照组 70例 ) ,治疗组服用健心平律丸 ,6g ,每天 3次 ;对照组服用胺碘酮 ,负荷量 60 0mg/d ,维持量2 0 0mg/d ,3 0天为 1疗程。应用阻断左冠状动脉造成大鼠心肌缺血再灌注损伤模型、心电图Ⅱ导联记录和水通道蛋白 4(AQP4)免疫组化染色方法观察健心平律丸对心肌缺血再灌注心律失常、死亡率、AQP4的影响。结果 :临床研究结果表明 ,健心平律丸的临床疗效、对不同类型心律失常的有效率、对各种主要症状改善率明显高于对照组 ,治疗组再住院率、心脏事件发生率、不良反应发生率低于对照组 ,二组比较有显著性差异 (P<0 .0 5、P <0 .0 0 5 )。实验研究结果表明 ,健心平律丸可明显减少再灌注心律失常发生率及死亡率 ,有上调缺血心肌AQP4表达水平的作用。结论 :健心平律丸具有治疗心律失常、抗心肌缺血再灌注心律失常的作用 ,可能与其上调缺血心肌AQP4表达水平 。

Objective:To explore the role of Jian-xin-ping-lu pellet on arrhythmia and expression of aquaporin 4 following myocardial ischemia-reperfusion injury of rats. Methods: 180 cases of arrhythmiawere randomly divided into Jian-xin-ping-lutreated group(treatment group) and Amiodarone treated group(control group).Jian-xin-ping-lu pelletwere administered to treatment group, 6 gram once, three times per day; Amiodarone were administered to control group,maxinum dose 600mg per day, keeping dose 200mg per day,30 days as one course oftreatment .Myocardial ischemia-reperfusion models were built by blocking left coronary artery. Ⅱlead of electrocardiogram HE stain and the expression of AQP4 measured by immuno-histochemical method were used for the effect of Jian-xin-ping-lu pellet.Results:Clinical study shows the effective rate to various arrhythmiaand improving role to clinicalmain symptomswere obviously higher in treatment group than those in control group. There were lower incidence of re-hospitalization , heart eventsand adverse drug reactions in treatment group than in control group.There were significant difference between the two groups(P<0.05,P<0.005). It alleviated ischemic myocardium edema injury and enhanced the expression of AQP4 in myocardium.Conclusion:Jian-xin-ping-lu pellet may play a role of antiarrhythmia in myocardial ischemia-reperfusion. It has a close relationship with the up-regulation of AQP4 in ischemia myocardium and abatement of intracellular edema.