January C T, Chau V, Makielski J C
Department of Medicine (Cardiology), University of Chicago, Illinois 60637.
Eur Heart J. 1991 Dec;12 Suppl F:4-9. doi: 10.1093/eurheartj/12.suppl_f.4.
The arrhythmogenic effects of ischaemia and reperfusion result from the complex interplay of normal ion channels reacting to the ischaemic environment, channels made abnormal by ischaemic modification, the appearance of new currents normally not present, and possible ischaemic alteration of metabolic electrogenic processes. In this report the cellular mechanisms thought to underlie the different types of triggered activity will be discussed. The role of Ca2+ channels and Ca2+ 'window' current in the generation of early after-depolarizations (EADs) will be elucidated.
缺血和再灌注的致心律失常作用源于正常离子通道对缺血环境的反应、因缺血修饰而异常的通道、新出现的正常情况下不存在的电流以及代谢性电生过程可能的缺血性改变之间的复杂相互作用。在本报告中，将讨论被认为是不同类型触发活动基础的细胞机制。将阐明钙通道和钙“窗”电流在早期后除极（EADs）产生中的作用。
