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目的 探讨自主神经系统对犬急性缺血心肌跨室壁复极离散度的影响。方法 经结扎冠状动脉前降支制备犬急性心肌缺血动物模型 ,用单相动作电位 (MAP)记录技术 ,同步记录 12只开胸犬急性缺血的左心室游离壁心外膜心肌 (epicardium ,Epi)、中层心肌 (midmyocardium ,Mid)和心内膜心肌 (endocardium ,Endo)的MAP。对自主神经刺激前和刺激过程中 ,3层心肌的跨室壁复极离散度和早期后除极 (earlyafterdepolarization ,EAD)的发生率进行比较。 结果 缺血 10min后 ,起搏周长为 10 0 0ms ,在未刺激自主神经的情况下 ,跨室壁复极离散度为 (5 5± 8)ms ;刺激交感神经的过程中 ,跨室壁复极离散度增加到 (86± 15 )ms (P <0 0 1) ;迷走神经刺激过程中 ,跨室壁复极离散度为 (5 3± 9)ms,与刺激前跨室壁复极离散度 (5 5± 8)ms相比差异无显著性 (P >0 0 5 )。交感神经刺激前 ,2只 (17% )犬的中层心肌出现EAD ;交感神经刺激过程中 ,7只 (5 8% )犬的中层心肌出现EAD (P <0 0 1)。结论 (1)交感神经刺激可增加缺血心肌的跨室壁复极离散度 ,且易在中层心肌细胞诱发EAD ,两者可诱发室性心动过速 ;(2 )迷走神经刺激对缺血心肌的跨室壁复极离散度无明显影响
Objective To investigate the effect of autonomic nervous system on the transmural dispersion of acute ischemic myocardium in dogs. Methods The animal models of acute myocardial ischemia in canine were prepared by ligation of the anterior descending coronary artery. The epicardium of the left ventricular free wall of acute thoracodorsal canine was simultaneously recorded by single phase action potential (MAP) recording technique. Epi), midmyocardium (Mid) and endocardium (Endo). The transmural repolarization dispersion and the incidence of early afterdepolarization (EAD) in 3 layers of myocardium were compared before and during autonomic nerve stimulation. Results After 10 minutes of ischemia, the perimeter of the pacing was 10 0 ms. In the absence of autonomic nerve stimulation, the transmural dispersion of repolarization was (55 ± 8) ms. In the process of sympathetic stimulation, the transmural wall The repolarization dispersion increased to (86 ± 15) ms (P <0.01). During the vagus nerve stimulation, the transmural repolarization dispersion was (53 ± 9) ms, which was significantly different from that before stimulation (5 5 ± 8) ms, there was no significant difference (P> 0.05). EAD was observed in the middle myocardium of two dogs (17%) before sympathetic stimulation; EAD was found in the middle myocardium of seven dogs (58%) during sympathetic nerve stimulation (P <0.01). CONCLUSIONS: (1) Sympathetic nerve stimulation can increase the transmural repolarization dispersion of ischemic myocardium and induce EAD easily in the middle myocardial cells, both of which can induce ventricular tachycardia; (2) vagus nerve stimulation of ischemic myocardium Transmural repolarization dispersion had no significant effect