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目的探讨急性心肌缺血时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)的变化及其计算机仿真研究。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三层心肌细胞Ito、动作电位时程(APD)、TDR和心律失常的影响,并结合急性心肌缺血Ito离子流和TDR的变化,应用修正Luo-Rody参数进行计算机仿真。结果急性心肌缺血早期犬左室内中外三层心肌细胞的Ito离子流增大,APD缩短,均以心外膜层细胞最明显,TDR增加,诱发R-on-T早搏和室性心动过速,并经计算机仿真可以证实与临床一致的心电图特点。结论急性心肌缺血时Ito离子流增大,TDR增加,产生2位相折返,是多型性室性心动过速发生的重要机制,计算机仿真可以显示这些特点。
Objective To investigate the changes of transient outward potassium current (Ito) and transmural repolarization dispersion (TDR) in canine wedge tissue of dogs with acute myocardial ischemia and its computer simulation. Methods The model of wedge-shaped myocardial tissue in canine perfused canine was established. The simultaneous application of floating glass microelectrode and electrocardiogram was used to observe the effects of acute myocardial perfusion-less myocardial ischemia on Ito, action potential duration (APD) , TDR and arrhythmia, combined with the change of Ito ion flow and TDR in acute myocardial ischemia, the computer simulation was carried out by using the modified Luo-Rody parameters. Results In early canine myocardial ischemia, the Ito flux in the left and right ventricular myocardium increased and the APD shortened. All the cells in the epicardial layer were the most obvious, the TDR increased, the R-on-T premature beats and ventricular tachycardia were induced, And by computer simulation can confirm the consistent with the clinical ECG features. Conclusions Acute myocardial ischemia increases Ito flux, increases TDR, and produces 2-phase reentry, which is an important mechanism for the development of polymorphic ventricular tachycardia. Computer simulation can show these characteristics.