Answers are grounded in this paper and cite their sources.
This review highlights the critical role of calcium channels and window currents in the cellular mechanisms of early after-depolarizations and triggered arrhythmias during cardiac ischaemia.
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.
No takes yet. Share an insight, caveat, or question.
January et al. (1991) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: