摘要
目的 :临床试验表明 ,I类抗心律失常药物虽能抑制心肌梗塞病人的室性心律失常 ,但增加死亡率 ,而胺碘酮 (Ⅲ类药物 )可提高心肌缺血患者的生存率。心室中层肌细胞 (M细胞 )有其独特的电生理特性并在心律失常发生中起重要作用。方法 :采用细胞内玻璃微电极技术 ,用含胺碘硐或心律平的模拟缺血液灌流M细胞 ,了解在缺血情况下 ,两种药物分别对M细胞电生理有何影响。结果 :(1)犬左心室M细胞的动作电位呈现出与心外膜层肌细胞相似的峰 -谷 -穹窿 (spikeanddome)形态 ;动作电位时程 (APD)随基础起搏周长 (BCL)延长而明显延长 ,即频率依赖性。 (2 )模拟缺血使M细胞的静息电位 (RP)除极、动作电位幅值 (APA)和Vmax减小、APD缩短 ,其APD的频率依赖性减弱或消失。 (3)胺碘硐可延缓或减轻缺血引起的电生理变化。 (4 )心律平明显抑制M细胞的Vmax、APA ,并随频率加快而作用增强。进一步加重了缺血引起的动作电位参数的改变 ,并可造成传导延缓或阻滞。结论 :胺碘酮可减轻而心律平则加重缺血引起的M细胞的电生理改变。
objective: Although class Ⅰantiarrhythmic drugs could suppress ventricular arrhythmias, they increased mortality in survivors of myocardial infarction. Nevertheless, amiodarone could improve survival in such patients.The ventricular midmyocardial myocytes (M cells) displayed a unique electrophysiological characteristics and played an important role in the genesis of arrhythmia. Methods: The effects of amiodarone and propafenone on simulated ischemic canine M cells were studied by conventional intracellular microelectrode techniques. Results: The M cells characterized by long action potential duration(APD), steep APD-rate relation, spike-and-dome configuration, rapid rate of rise in upstroke(Vmax), and more negative resting potential(RP). The simulated ischamic M cells showed a reduced RP, action potential amplitude(APA), Vmax and APD. The APD rate-dependence also decreased or vanished. Adding amiodarone to simulated solution could delay and attenuated the electrophysiologic changes induced by ischemia. Propafenone inhibited the Vmax of M cells and this inhibition was rate-dependent. Propafenone aggravated the electrophysiologic effects of ischemia and could cause conduction delay or block. Conclusion: Amiodarone attenuated the electrophysiologic changes induced by ischemia, whereas propafenone aggravated it. This result could be possible explanation of the different effects of the two drugs on mortality of coronary heart disease patients.[
