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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: Slow response delayed rectifier potassium channels (IKs) is an important part of cardiomyocytes repolarization. In this study, the left ventricular hypertrophy of Ipi on subepicardial (Epi) and subendocardial endocardial (Endo) IKs mRNA expression levels Variety. Methods: Sixteen rabbits were randomly divided into sham operation group and cardiac hypertrophy group. Cardiac hypertrophy caused by a partial ligation of the abdominal aorta pressure overload rabbit model of cardiac hypertrophy, sham operation group only exposed the abdominal aorta without contracting. The mRNA expression of IKs channel genes KvLQT1 (α subunit) and minK (β subunit) was detected by RT-PCR. Results: KvLQT1 of EpiIKs channel was 2.5 times that of Endo, and minK of EpiIKs channel β subunit was 3.3 times of Endo. Compared with the sham-operated group, the expression of KvLQT1 in Epi and EndoIKs channels decreased by 40% and 25% respectively in cardiac hypertrophy group, and 50% and 33% in myocardial hypertrophy group respectively. Conclusion: The mRNA expression of IKs channel genes KvLQT1 and minK is different across the wall. Cardiac hypertrophy results in a non-uniform decrease in mRNA expression of Epi and EndoIKs.