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目的:探讨缺血性T波电交替(TWA)的电生理学机制。方法:在体实验组家兔10只,开胸后结扎左冠状动脉前降支(LAD),造成心肌缺血模型,在结扎LAD前、结扎后60min重复观测缺血区域心室壁内膜下层、中层和外膜下层的单相动作电位时程(MAPD)、有效不应期(ERP),快速心室刺激诱发TWA。离体实验组家兔10只,快速开胸取出心脏后作Langendorff灌流,先用正常Tyrode’s液灌流30 min再用模拟缺血液灌流。在Tyrode’s液灌流20min后、模拟缺血液灌流60min后重复观测模拟肢体导联心电图,以及左心室前壁、侧壁、右心室和心尖部心外膜的MAPD、ERP,快速心室刺激诱发TWA。结果:缺血后各位点MAPD的频率适应性降低,MAPD90和ERP缩短。与生理状态相比,心肌细胞复极梯度发生了明显重排。20个在体和离体心脏在缺血后全部可用快速心室刺激诱发TWA,诱发TWA的心动周期(CL)窗口在130-170ms之间,CL=140,150ms时可稳定地诱发TWA。TWA时伴有单相动作电位复极和传导的交替。离体心外膜增频刺激时,CL=170 ms开始出现TWA,随后的减频刺激至CL=200ms时TWA消失,即TWA的滞后现象。结论:心肌细胞复极不均一可能是引起心电图T波的原因之一。心肌缺血使心脏正常的复极梯度发生改变,在快速心室刺激时易于发生动作电位复极和传导的交替,在体表心电图上表现为TWA。
Objective: To investigate the electrophysiological mechanism of ischemic T wave alternation (TWA). Methods: Ten rabbits in the experimental group were subjected to thoracotomy and ligation of the left anterior descending coronary artery (LAD) to establish a model of myocardial ischemia. Before the LAD was ligated, the inferior ventricular wall of the ischemic area was observed 60 minutes after ligation, Middle and epicardial monophasic action potential duration (MAPD), effective refractory period (ERP), rapid ventricular stimulation induced TWA. Ten rabbits in the experimental group were given Langendorff perfused immediately after thoracotomy. The hearts were perfused with normal Tyrode’s solution for 30 minutes and then simulated ischemia. After 20 min of Tyrode’s liquid perfusion, the electrocardiogram of mimic limb lead and the MAPD, ERP of the left ventricular anterior, epicardial and apical epicardium were observed after 60 min perfusion. TWA was induced by rapid ventricular stimulation. Results: The frequency adaptability of MAPD decreased at each site after ischemia, and MAPD90 and ERP shortened. Compared with the physiological state, cardiomyocyte repolarization gradient obvious rearrangement occurred. TWA was induced by rapid ventricular stimulation in all 20 isolated and isolated hearts after ischemia, and TWA was induced within 130-170 ms in TWA window. TWA was induced at CL = 140 and 150 ms. TWA accompanied by single-phase action potential repolarization and conduction of alternating. Excitation of isolated epicardium stimulated TWA began at CL = 170 ms, and then TWA disappeared at CL = 200 ms after TWA stimulation, ie, the lag of TWA. Conclusion: Inhomogeneous repolarization of cardiomyocytes may be one of the causes of T wave of electrocardiogram. Myocardial ischemia changes the normal repolarization gradient of the heart, which is prone to alternating repolarization and conduction of action potentials during rapid ventricular stimulation. It appears as TWA on the body surface electrocardiogram.