表没食子儿茶素没食子酸酯对缺血性心律失常的影响

Effect of EGCG on ischemic arrhythmia

目的 探讨表没食子儿茶素没食子酸酯（epigallocatechin gallate,EGCG）对缺血性心律失常的影响及作用机制。方法 选取3~4月龄Wistar大鼠80只,采用以5μg/kg剂量尾静脉注射乌头碱生理盐水溶液,建立缺血性心律失常模型,灌胃给药6 d,随机分为假手术组、模型组、低剂量组及高剂量组。记录给药后30 min内各实验组大鼠心电图变化,室性早搏（ventricular premature beat,VPB）次数和首次出现时间,室性心动过速（ventricular tachycardia,VT）和心室颤动（ventricular fibrillation,VF）次数和持续时间;Evans blue染色计算心肌梗死率;股动脉采血,分离血清,测定乳酸脱氢酶（lactic dehydrogenase,LDH）及肌酸激酶同工酶（creatine kinase MB,CK-MB）。结果 与假手术组比,模型组出现缺血性心律失常,VPB、VT和VF频数明显增加（P〈0.05）,大鼠室速和室颤程度显著加重（P〈0.05）,心肌梗死率明显增加（P〈0.05）,LDH和CK-MB表达也明显升高（P〈0.05）;与模型组相比,经过EGCG治疗后,大鼠的心律失常明显改善（P〈0.05）,VPB,VT和VF频数明显减少（P〈0.05）,VPB首发时间推迟（P〈0.05）,VT和VF持续时间缩短（P〈0.05）,心肌梗死率下降（P〈0.05）,LDH、CK-MB表达也明显下降（P〈0.05）,高剂量组比低剂量组更明显。结论 EGCG能明显改善缺血引起的心律失常,其作用机制与血清中LDH和CK-MB的表达相关。

Objective To investigate the effect of epigallocatechin gallate （EGCG） on ischemie arrhythmia and its mechanism. Methods Eighty cases of 3 -4 month old Wistar rats were selected, the ischemie arrhythmia model was established by 5 μg/kg dose of intravenous injection of aconitine in normal saline solution with continuous intragastric administration for 6 days, and then randomly divided into sham operation group, model group, high dose group and low dose group. ECG changes, times and first time of VPB, the frequency and duration of ventricular tachycardia （VT） and ventricular fibrillation （VF） were recorded within 30 min after administration of EGCG. Myocardial infarction rate was calculated by Evans blue staining, lactate dehydrogenase （LDH） and ereatine kinase （CK-MB） were determined after femoral artery punctured and isolated from serum. Results Compared with sham group, ischemic arrhythmia changes occurred in the model group. VPB, VT and VF frequency increased significantly （P 〈 0. 05）, rat ventrieular tachycardia and ventricular fibrillation degree were significantly increased （P 〈 0. 05 ）, myocardial infarction rate increased （ P 〈 0. 05 ）, and CK-MB and LDH expression increased significantly （P 〈 0. 05 ）. Compared with the model group, EGCG obviously improved ischemic arrhythmia in rats （ P 〈 0.05 ）, significantly reduced the VPB, VT and VF frequency （ P 〈 0. 05 ）, delayed VPB starting time （ P 〈 0.05 ）, shortened the duration （P 〈 0. 05） of VT and VF, myocardial infarction rate and LDH, CK, CK-MB expression also decreased significantly （P 〈 0. 05 ）, high dose group was more obviously than the low dose group. Conclusion EGCG can significantly improve the ischemia and induce the arrhythmia, and the mechanism is related to the expression of LDH and CK-MB in serum.