急性心肌缺血犬心肌细胞瞬时外向钾电流和跨壁复极离散度变化致心律失常机制研究

目的:探讨急性心肌缺血对犬左室心肌楔形组织块瞬时外向钾电流(Ito)、跨壁复极离散度(TDR)变化及其与室性心律失常的关系。方法:建立冠状小动脉灌注犬左室心肌楔形组织块模型,应用浮置玻璃微电极和心电图同步记录技术,观察急性无灌流心肌缺血对内、中、外3层心肌细胞Ito、动作电位时程(APD)、TDR和心律失常的影响。结果:急性心肌缺血早期犬左室内、中、外3层心肌细胞的Ito增大,APD缩短,均以外膜心肌细胞最明显,TDR增加,诱发早期后除极、R-on-T期前收缩和室性心动过速。结论:急性心肌缺血时Ito增大,TDR增加,产生2相位折返,是多型性室性心动过速发生的重要机制。

Study on mechanism of arrhythmogenesis and the changes of Ito and transmural dispersion of repolarization during acute myocardial ischemia in canine

Objective:To explore the role of acute ischemia on transient outward potassium current (I_ to ), transmural dispersion of repolarization (TDR) and ventricular arrhythmia in canine left ventricular wedge. Method:Observing the role of acute non-flow cardiac ischemia on I_ to , action potential duration (APD ) of Epi, Mid and Endo-myocardial cells, TDR and arrhythmia in arterially perfused canine left ventricular wedge preparation by using floating glass microelectrode and recording electrocardiogram at the same time. Result:After 10 minutes acute ischemia, in canine left ventricular wedge preparation, APD of three layer cells shortens and I_ to increases simultaneously, especially in Epi; TDR and I_ to are increased; Delayed afterdepolarization (DAD), R on T premature beat and ventricular tachycardia are induced. Conclusion:Acute cardiac ischemia cause an increase in TDR and I_ to in arterially perfused canine left ventricular wedge preparation, and inducing phase 2 reentry is an important mechanism of polymorphous ventricular tachycardia (PMVT) onset.