自主神经对急性缺血心肌跨室壁复极离散度影响的实验研究

Experimental study of the effect of autonomic nervous system on the transmural dispersion of ventricular repolarization under acute myocardial ischemia in vivo

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 )

Objective To investigate the effect of the autonomic nervous system on the transmural dispersion of ventricular repolarization(TDR) under acute myocardial ischemia in intact canine.Methods Acute myocardial ischemia models were prepared by ligating the left anterior descending coronary artery,and the monophasic action potentials(MAPs) of the epicardium(Epi),midmyocardium(Mid) and endocardium(Endo) in the left ventricular free wall were recorded simultaneously by specially designed plunge needle electrodes at baseline and under myocardial ischemia in 12 open chest dogs.MAPD 90 and TDR among the three myocardial layers were compared,so as the incidence of the early afterdepolarization(EAD) before and during autonomic nerve stimulation.Results After ten minutes of acute myocardial ischemia,TDR was increased from(55±8) ms to (86±15) ms during sympathetic nerve stimulation ( P <0 01).There is no significant difference between the TDR(53±9) ms during parasympathetic nerve stimulation and that of the baseline(55±8) ms ( P >0 05).The EAD of 2 dogs(17%) were elicited in the Mid layer at 10 minutes after acute myocardial ischemia,and 7 dogs(58%) in the Mid layer during sympathetic nerve stimulation( P <0 01).Conclusion The sympathetic nerve stimulation may increase the TDR and induce the EAD in the Mid layer under acute myocardial ischemia,whereas the parasympathetic stimulation seems not to affect the TDR under acute myocardial ischemia.