Mitochondrial depolarization and electrophysiological changes during ischemia in the rabbit and human heart

Matthew S. Sulkin, Bas J. Boukens, Megan Tetlow, Sarah R. Gutbrod, Fu Siong Ng, Igor R. Efimov*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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. The present study was designed to resolve the aforementioned difference and determine the unknown relationship between ΔΨm and electrophysiology. We developed a novel imaging modality for simultaneous optical mapping of ΔΨm and transmembrane potential (Vm). Optical mapping was performed using potentiometric dyes on preparations from 4 mouse hearts, 14 rabbit hearts, and 7 human hearts. Our data showed that during ischemia, ΔΨm depolarization is sporadic and changes asynchronously with electrophysiological changes. Spatially, ΔΨm depolarization was associated with action potential duration shortening but not conduction slowing. Analysis of focal activity indicated that ΔΨm is not different within the myocardium where the focus originates compared with normal ventricular tissue. Overall, our data suggest 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.

Original languageEnglish (US)
Pages (from-to)H1178-H1186
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number8
StatePublished - Oct 15 2014


  • Arrhythmia
  • Imaging
  • Ischemia
  • Metabolism

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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