论文部分内容阅读
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.
OBJECTIVE: To study the changes of KCNE1 and KCNE2 gene expression in ischemic myocardium of rats and further explore the mechanism of arrhythmia after acute myocardial infarction.Methods: Acute myocardial infarction model of SD rats was successfully established and detected by RT-PCR and Western blotting The levels of KCNE1 and KCNE2 mRNA and protein in ischemic myocardium at 24 h, 1, 2 and 4 wk after AMI were observed, and the incidence of ventricular arrhythmia in each group was observed.Results: KCNE1 and KCNE2 The mRNA and protein expression of KCNE1 and KCNE2 in ischemic myocardium increased significantly (P <0.05) 24h after acute myocardial infarction and peaked at 1-2wk, then began to decline. At 4wk, KCNE1 MRNA and protein levels and mRNA level of KCNE2 were still significantly higher than those in normal myocardium (P <0.05) .In addition, myocardial infarction model group, especially 1wk and 2wk group after myocardial infarction significantly more ventricular arrhythmia than sham operation Group.Conclusion: The abnormal changes of gene expression of KCNE1 and KCNE2 in ischemic myocardium after acute myocardial infarction may affect the self-discipline, excitability and conductivity of cardiomyocytes, and become the post-infarction heart rhythm One of the reasons often generated.