摘要
目的 :探讨心肌肥厚易致心律失常的机制。 方法 :用 L-甲状腺素制备大鼠心肌肥厚模型 ,定量逆转录PCR方法 ( RT-PCR)测定肥厚心肌内电压依赖性 K+ 通道 m RNA含量。 结果 :与正常对照组相比 ,肥厚心肌内电压依赖性 K+ 通道 m RNA的表达水平下降 42 % ( 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+ 通道转录水平下降 ,可能会导致动作电位复极化时间延长 。
Objectives: To understand the molecular mechanisms of electrophysiological alterations underlying cardiomyocyte hypertrophy. Methods: Expression of cardiac voltage-gated K+ channel genes was examined in ventricles of L-thyroxin-induced cardiac hypertrophy rats. This study quantified voltage-gated K+ channel mRNA by reverse transcription and polymerase chain reaction amplification. Results: Compared with control group, the expressions of voltage-gated K+ channels mRNA were significantly decreased by 42%(P<0.05). Conclusions:The electrophysiological alterations may be associated with transcriptional regulation of voltage-gated K+ channels. These findings provide, at least in part, the molecular basis for electrophysiological alterations under hypertrophy.
出处
《医学研究生学报》
CAS
2000年第4期213-215,共3页
Journal of Medical Postgraduates