Fujinaga H, Wakatsuki T, Nishikado A, Oki T, Ito S
Second Department of Internal Medicine, School of Medicine, University of Tokushima, Japan.
Coron Artery Dis. 1998;9(10):697-701.
There have been few studies concerning the electrophysiologic changes associated with the use of angiotensin-converting enzyme inhibitors in patients with acute myocardial infarction. We examined the electrophysiologic effects of quinaprilat in dogs during acute myocardial ischemia and following reperfusion.
The left anterior descending coronary artery was occluded for 10 min and reperfused for 10 min. Animals received intravenous quinaprilat (3 micrograms/kg per min, quinaprilat group) or saline (control group). We measured the ventricular effective refractory period and intra-myocardial conduction time within the left anterior descending coronary artery region (ischemic region) during myocardial ischemia and following reperfusion, and determined the frequency of ventricular fibrillation.
The effective refractory period in the ischemic region decreased during myocardial ischemia and decreased further immediately after reperfusion in the control group. The intra-myocardial conduction time in the ischemic region increased during myocardial ischemia but rapidly shortened after reperfusion in the control group. In the quinaprilat group, however, no significant differences were evident between the ischemic and non-ischemic regions in either the effective refractory period or the intra-myocardial conduction time during myocardial ischemia or following reperfusion. The percentage shortening of the effective refractory period and the percentage prolongation of the intra-myocardial conduction time in the ischemic region were significantly lower in the quinaprilat group than in the control group during myocardial ischemia and following reperfusion. The frequency of ventricular fibrillation during myocardial ischemia and following reperfusion was significantly lower in the quinaprilat group (21%) than in the control group (74%; P < 0.01).
Quinaprilat protects against electrophysiologic abnormalities, and may decrease arrhythmias during acute myocardial ischemia and following reperfusion.
关于急性心肌梗死患者使用血管紧张素转换酶抑制剂相关的电生理变化的研究较少。我们研究了喹那普利拉在犬急性心肌缺血及再灌注过程中的电生理作用。
结扎左冠状动脉前降支10分钟，然后再灌注10分钟。动物分为静脉注射喹那普利拉组（3微克/千克每分钟，喹那普利拉组）和生理盐水组（对照组）。我们测量了心肌缺血及再灌注过程中左冠状动脉前降支区域（缺血区）的心室有效不应期和心肌内传导时间，并测定室颤发生率。
对照组中，缺血区有效不应期在心肌缺血时缩短，再灌注后立即进一步缩短。缺血区心肌内传导时间在心肌缺血时延长，但再灌注后迅速缩短。然而，在喹那普利拉组，心肌缺血及再灌注期间，缺血区与非缺血区在有效不应期或心肌内传导时间方面均无明显差异。喹那普利拉组缺血区有效不应期缩短百分比及心肌内传导时间延长百分比在心肌缺血及再灌注期间均显著低于对照组。喹那普利拉组心肌缺血及再灌注期间室颤发生率显著低于对照组（21%比74%；P<0.01）。
喹那普利拉可预防电生理异常，可能减少急性心肌缺血及再灌注期间的心律失常。
