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一氧化碳在实验性急性心肌缺血中的致心律失常作用:不存在传导减慢和室性心动过速。

Arrhythmogenic effects of carbon monoxide in experimental acute myocardial ischemia: lack of slowed conduction and ventricular tachycardia.

作者信息

Foster J R

出版信息

Am Heart J. 1981 Nov;102(5):876-82. doi: 10.1016/0002-8703(81)90039-9.

DOI:10.1016/0002-8703(81)90039-9
PMID:7304396
Abstract

To investigate the possibility that carbon monoxide (CO) at high clinically encountered levels may have arrhythmogenic effect in initial minutes of acute myocardial ischemia, 14 dogs underwent thoracotomy and recording of bipolar epicardial electrograms during brief (6-minute) left anterior descending coronary artery (LAD) occlusions. Eight of the 14 dogs were studied both before and after CO pretreatment in which carboxyhemoglobin levels of 6.8% to 14.6% (mean 10.4 +/- 2.8%) were achieved. Epicardial electrograms showed no change in degree of ischemic myocardial conduction slowing after CO, and there was no significant difference between CO and no-CO LAD occlusions in incidence of spontaneous ventricular tachycardia. Since the degree of myocardial conduction slowing is thought to be importantly related to susceptibility to ventricular arrhythmias in acute ischemia, this study suggests that CO may not be arrhythmogenic during early minutes of acute myocardial ischemia.

摘要

为了研究临床上常见的高浓度一氧化碳(CO)在急性心肌缺血最初几分钟内是否具有致心律失常作用,对14只犬进行开胸手术,并在短暂(6分钟)左冠状动脉前降支(LAD)闭塞期间记录双极心外膜电图。14只犬中的8只在CO预处理前后均进行了研究,预处理后羧基血红蛋白水平达到6.8%至14.6%(平均10.4 +/- 2.8%)。心外膜电图显示,CO处理后缺血心肌传导减慢程度无变化,CO处理组与未处理组LAD闭塞后自发性室性心动过速的发生率无显著差异。由于心肌传导减慢程度被认为与急性缺血时对室性心律失常的易感性密切相关,本研究表明,在急性心肌缺血的早期几分钟内,CO可能不具有致心律失常作用。

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