摘要
目的:研究大鼠缺血心肌中KCNE1,KCNE2基因表达变化情况,进一步探讨急性心肌梗死后并发心律失常的机制.方法:成功建立SD大鼠急性心肌梗死模型,通过RT-PCR、免疫印迹方法检测急性心肌梗死后24h及1,2,4wk梗死周边缺血心肌中KCNE1,KCNE2mRNA和蛋白质的水平,并观察各组室性心律失常的发生情况.结果:SD大鼠左室心肌中有KCNE1及KCNE2的表达,在急性心肌梗死后24h,无论是KCNE1还是KCNE2的mRNA和蛋白质表达在缺血心肌中均呈明显增加(P<0.05),并在1～2wk达到高峰,随后开始下降,4wk时KCNE1的mRNA、蛋白质水平和KCNE2的mRNA水平仍显著高于正常心肌中的表达(P<0.05).此外,心梗模型各组尤其是心肌梗死后1wk和2wk组室性心律失常明显多于假手术组.结论:急性心肌梗死后缺血心肌中KCNE1,KCNE2这两个离子通道基因表达的异常变化,可能对心肌细胞的自律性、兴奋性和传导性产生影响,成为梗死后心律失常产生的原因之一.
AIM：To investigate the dynamic changes of KCNE1,KCNE2 gene expression in acute ischemic myocardium of rat,and to explore the mechanism of cardiac arrhythmia after acute myocardial infarction（AMI）.METHODS：Acute myocardial infarction model of Sprague-Dawley rat was successfully established.KCNE1,KCNE2 mRNA and protein levels were detected in ischemic myocardium using reverse transcriptase PCR and Western blotting 24 h,1,2 and 4 weeks after the establishment of AMI model,and ventricular arrhythmia was detected using ECG in all groups.RESULTS：The expression level of both KCNE1 and KCNE2 increased significantly in ischemic myocardium（P0.05） 24 h after AMI,achieving highest level within 1-2 weeks,and then decreased.Nevertheless,the mRNA and protein level of KCNE1 and KCNE2 remained significantly higher in ischemic myocardium 4 weeks after AMI,compared with that in myocardium of control group（P0.05）.The incidence of ventricular arrhythmia was significantly higher in AMI groups than in sham operation group,especially during the period from 1 week to 2 week after the establishment of AMI model.CONCLUSION：The increased expression level of KCNE1 and KCNE2 gene in ischemic myocardium after acute myocardial infraction may have influence on the electrophysiological characteristics of these two ionophorous protein,resulting in the alteration of auto-rhythmicity,excitability and conductivity of myocardial cells,and therefore inducing cardiac arrhythmia after acute myocardial infarction.
出处
《第四军医大学学报》
北大核心
2009年第24期2974-2977,共4页
Journal of the Fourth Military Medical University
基金
重庆市科委（CSTC,2008BB5077）对本课题完成的资助.
