利多卡因能相对延长心肌有效不应期吗?

Does lidocaine prolong effective refractory period of myocardium relatively?

利多卡因抗心律失常的主要机制是抑制晚钠电流(I_(Na-L)),其缩短动作电位时程(APD)被认为是通过相对延长有效不应期(ERP),使更多的异位激动落在该期而失去作用,从而作为抗心律失常的一部分。然而,I_(Na-L)持续时间较长甚至其通道不失活,且心肌复极到-60 mV左右,内向整流K+通道开放,加速复极完成。外向阳离子流的增大削弱I_(Na-L)的影响致其作用并不明显。故利多卡因缩短APD更多的是缩短ERP,使ERP在APD中所占的比值下降并成为其致心律失常的基础,而不是相对延长ERP。其抗心律失常的主要作用在于抑制I_(Na-L)且恢复损伤细胞内外极性,提高心肌兴奋阈值,降低其兴奋性。

The anti-arrhythmic mechanism of lidocaine is mainly to inhibit the late Na＋ current （INa-L）, by whichmyocardial action potential duration （APD） is shortened, leading to the relative extension of effective refractory period（ERP）. Therefore, more ectopic excitation will locate in ERP so as to lose their effect of initiating action potential.However, long opening time or un-inactivation of INa-L induced by lidocaine may cause rectifier K＋ channels open whencardiomyocyte repolarizes to -60 mV, which eventually leads to accelerated repolarization. Thus, the enhanced outwardK＋ current may reduce the effect of lidocaine-induced INa-L inhibition on APD. In summary, the final effect of lidocaineto shorten APD is to reduce ERP, which induces the reduction of the percentage of ERP in APD and eventually causesarrhythmia, but not extends ERP relatively. The mechanism of lidocaine in anti-arrhythmia is to inhibit INa-L and recoverthe polarization of damaged cells, which may increase the exciting threshold and decrease the excitation ability ofcardiomyocyte.