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急性心肌缺血及室性心律失常的相关性已在实验动物得以证实。kaplinsky等发现狗冠状动脉闭塞30分钟内,早期室性心律失常的两个时期。Janse等描述了急性实验性心肌缺血时,心室节律异常的两种机制。他们发现,在缺血边缘的正常面存在一个病灶机制,可能由于正常浦肯野纤维内损伤电流所致,然而,在缺血心肌发现由大、小折返径而致的室性心律失常。猫冠状动脉闭塞后出现心肌及心外膜区域传导时间延长,非同步去极化及不应期缩短伴有室性心律失常。Kabell等证实:在实验动物,侧枝血流进入梗塞区减少而致的缺血可使梗塞区电图分级和延迟,以
The association between acute myocardial ischemia and ventricular arrhythmias has been demonstrated in experimental animals. Kaplinsky et al found that dogs with coronary artery occlusion within 30 minutes of early ventricular arrhythmia in two periods. Janse et al describe two mechanisms of abnormal ventricular rhythm in acute experimental myocardial ischemia. They found that there is a focal mechanism at the normal side of the ischemic margin, which may be due to a lesion current in normal Purkinje fibers. However, ventricular arrhythmias induced by large and small foldback were found in the ischemic myocardium. Cardiac and epicardial areas of the cat after coronary occlusion lead to longer conduction time, non-synchronized depolarization and refractory period associated with ventricular arrhythmias. Kabell et al confirmed that in experimental animals, ischemia of the collateral flow into the infarct area may grade and delay the infarction area electrogram