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室性心律失常通常因运动或情绪应激诱发,特别是在先天性长QT综合征(LQTS)的患者。运动或情绪应激刺激交感神经系统,主要引起心脏β-肾上腺素受体的激活。快速激活延迟整流钾电流(IKr)在心肌动作电位的复极过程中发挥关键的作用,IKr的减弱可延长心肌动作电位时程,导致LQTS。研究发现,抑制HERG/IKr电流,导致心脏复极延长,这对应激增加致死性心律失常的发生提供了一个病理生理的解释。现就β-肾上腺素受体对HERG钾通道调控机制及其临床意义作一综述。
Ventricular arrhythmias are usually induced by exercise or emotional stress, especially in patients with congenital long QT syndrome (LQTS). Exercise or emotional stress stimulates the sympathetic nervous system, mainly resulting in the activation of cardiac β-adrenergic receptors. Rapid activation of delayed rectifier potassium current (IKr) plays a key role in the repolarization of myocardial action potentials. IKr weakening prolongs myocardial action potential duration and leads to LQTS. The study found that inhibition of HERG / IKr currents leads to prolonged cardiac repolarization, which provides a pathophysiological explanation for the increased stress-induced lethal arrhythmia. Now β-adrenergic receptor HERG potassium channel regulation mechanism and its clinical significance are reviewed.