兔肥厚心肌慢反应延迟整流钾通道表达的变化

Changes of expression of slowly activating delayed rectifier potassium channel in rabbits with cardiac hypertrophy

目的:慢反应延迟整流钾通道(IKs)是心肌细胞复极的重要组成部分,本实验观察左心室肥厚对心外膜下心肌(Epi)和心内膜下心肌(Endo)IKs的mRNA表达水平变化。方法:家兔16只随机分为假手术组和心肌肥厚组。心肌肥厚组通过部分结扎腹主动脉的方法造成兔压力负荷性心肌肥厚模型,假手术组只暴露腹主动脉而不行缩窄术。应用RT-PCR技术检测IKs通道基因KvLQT1(α亚单位)和minK(β亚单位)的mRNA表达。结果:假手术组EpiIKs通道α亚单位基因KvLQT1为Endo的2.5倍,EpiIKs通道β亚单位基因minK为Endo的3.3倍。与假手术组相比,心肌肥厚组Epi和EndoIKs通道α亚单位基因KvLQT1表达分别降低40%和25%,心肌肥厚组Epi和EndoIKs通道β亚单位基因minK表达分别降低50%和33%。结论:IKs通道基因KvLQT1和minK的mRNA表达存在跨室壁的差异。心肌肥厚可造成Epi和EndoIKs的mRNA表达不均一的下降。

Objective：Slowly activating delayed rectifier potassium currents（IKs）are the main component of the repolarization of cardiac myocytes.The present study was to evaluate the effects of left ventricular hypertrophy（LVH）on the mRNA level of IKs of both epicardial and endocardial myocytes.Method：A total of 16 rabbits were divided randomly into sham group and LVH group.LVH was induced by partial ligation of abdominal aorta.Sham group underwent a similar surgical procedure without aortic ligation.Expression of KvLQT1（α-subunit of IKs）and minK（β-subunit of IKs）was measured by the RT-PCR technique.Result：In the sham group,expression of KvLQT1（α-subunit of IKs）was 2.5 times in epicardium than endocardium,while expression of minK（β-subunit of IKs）was 3.3 times in epicardium than endocardium.Compared with sham group,in LVH group,expression of KvLQT1（α-subunit of IKs）was decreased 40% and 25% in epicardium and endocardium,respectively,while expression of minK（β-subunit of IKs）was decreased 50% and 33% in epicardium and endocardium,respectively.Conclusion：There are transmural differences in the expression of KvLQT1 and mink,which encode IKs.LVH could cause inhomogeneities of the mRNA expression of IKs reduced between endocardium and epicardium.