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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。
Myocardial outward delayed rectifier K + current IK can be divided into IKr, IKs and IKur3 kinds of components or sub-current, its change is one of the important causes of arrhythmia caused by pathological conditions. Myocardial hypertrophy IKr, IKs decreased lead to action potential time (APD) prolonged, for the early depolarization (EAD) and TdP created the preconditions. Increased IKr, IKs, and IKur during ischemia and sympathetic nerve activation can lead to increased heterogeneity of APD and arrhythmia. Most class III anti-arrhythmic drugs mainly block IKr, easily lead to excessive prolongation of APD, induced EAD, TdP and other arrhythmias. The blockade of IKs by composite class III antiarrhythmic drugs not only favors antiarrhythmic but also reduces adverse effects.