Abstract
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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
