摘要
心肌外向延迟整流K+电流IK 可分为IKr、IKs和IKur3种成分或亚电流 ,它的变化是在病理情况下引起心律失常的重要原因之一。心肌肥厚时IKr、IKs的减少导致动作电位时间(APD)延长 ,为早后除极 (EAD)和TdP的产生创造了前提条件。缺血和交感神经兴奋时IKr、IKs和IKur的增加可导致APD异质性加大 ,促发心律失常。多数Ⅲ类抗心律失常药物主要阻断IKr,易导致APD过度延长 ,诱发EAD、TdP等心律失常。复合性Ⅲ类抗心律失常药对IKs的阻断不仅有利于抗心律失常 ,而且也能减少不良反应。
Cardiac outward delayed rectifier current may be divided into three subtypes:I Kr ,I Ks and I Kur .The alterations of I K in pathological process is one of the main mechanisms in arrhythmia.The I Kr and I Ks are reduced in hypertrophied cardiac muscle,which lead to prolongation of action potential duration and provide conditions for early after depolarization and TdP.Ischemia and(or) over sympathetic activity may result in the increase of I Kr ,I Ks and I Kur ,which may give rise to arrhythmia by generating dispersion of repolarization between ventricles.Most class Ⅲ antiarrhythmic agents mainly block I Kr ,and augment dispersion of depolarization and induce arrhythmias.Multiple ionic channel blockers have been chosen for their minimum reverse reaction and low incidence of clinical TdP arrhythmias.
出处
《东南大学学报（医学版）》
CAS
2003年第5期344-349,共6页
Journal of Southeast University(Medical Science Edition)
基金
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