Document Detail

Mitochondrial depolarization and electrophysiological changes during ischemia in the rabbit and human heart.
MedLine Citation:
PMID:  25128175     Owner:  NLM     Status:  Publisher    
Instability of the inner mitochondrial membrane potential (ΔΨm) has been implicated in electrical dysfunction, including arrhythmogenesis during ischemia/reperfusion. Monitoring ΔΨm has led to conflicting results, where depolarization has been reported as sporadic and as a propagating wave. This study was designed to resolve the aforementioned differences and determine the unknown relationship between ΔΨm and electrophysiology. We developed a novel imaging modality for simultaneous optical mapping (OM) of ΔΨm and transmembrane potential (Vm). OM was performed using potentiometric dyes on preparations from 4 mouse, 14 rabbit, and 7 human hearts. Our data shows that ischemia causes sporadic ΔΨm depolarization, while propagating waves are an artifact created by ischemia-induced contracture of the heart. During ischemia, electrophysiological changes are asynchronous with ΔΨm depolarization. Spatially, ΔΨm depolarization is associated to action potential duration shortening, but not conduction slowing. Analysis of focal activity indicates that ΔΨm is not different within myocardium where the focus originates compared to normal ventricular tissue. Overall, our data suggests that during ischemia mitochondria maintain their function at the expense of sarcolemmal electrophysiology, but ΔΨm depolarization does not have a direct association to ischemia-induced arrhythmias.
Matthew S Sulkin; Bastiaan J Boukens; Megan Tetlow; Sarah R Gutbrod; Fu Siong Ng; Igor R Efimov
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-8-15
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  -     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2014 Aug 
Date Detail:
Created Date:  2014-8-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014, American Journal of Physiology - Heart and Circulatory Physiology.
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