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目的 :探讨心肌肥厚易致心律失常的机制。 方法 :SD大鼠实验组 9只 ,对照组 7只 ,用 L -甲状腺素诱导法制备大鼠心肌肥厚模型 ,用逆转录多聚酶链反应方法(RT- PCR)半定量分析肥厚心肌内电压依赖性 K+ 通道信使核糖核酸 (m RNA)水平。 结果 :实验组与对照组相比 ,实验组即肥厚心肌内电压依赖性 K+ 通道 m RNA的表达水平显著下降 (P<0 .0 5 )。 结论 :电压依赖性 K+ 通道是心肌电活动的主要离子通道 ,心肌肥厚时电压依赖性 K+ 通道基因表达水平下降 ,可能会导致动作电位复极化时间延长 ,与易诱发心律失常有关
Objective: To investigate the mechanism of cardiac hypertrophy induced arrhythmia. Methods: Nine rats in experimental group and seven in control group were induced by L - thyroxine to induce myocardial hypertrophy in rats. Reverse transcription - polymerase chain reaction (RT - PCR) was used to semi - quantitatively analyze the voltage - dependent K + channel messenger RNA (m RNA) levels. Results: Compared with the control group, the expression of voltage-dependent K + channel m RNA in hypertrophic myocardium in experimental group was significantly decreased (P <0.05). Conclusion: The voltage-dependent K + channel is the main ion channel of cardiac electrical activity. Decreased voltage-dependent K + channel gene expression in cardiac hypertrophy may lead to prolonged repolarization of action potential, which may be associated with easily induced arrhythmia