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Related Experiment Videos

Regional gap junction inhibition increases defibrillation thresholds.

J Jason Sims1, Kell L Schoff, Jennifer M Loeb

  • 1School of Pharmacy, University of Wisconsin, Madison, WI 53705, USA. jjsims@pharmacy.wisc.edu

American Journal of Physiology. Heart and Circulatory Physiology
|March 8, 2003
PubMed
Summary

Regional gap junction inhibition during ischemia increases defibrillation thresholds (DFT) by slowing conduction velocity and increasing its dispersion. This suggests impaired gap junction function is a key factor in defibrillation failure during ischemia.

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Area of Science:

  • Cardiovascular Physiology
  • Electrophysiology
  • Medical Device Technology

Background:

  • Ischemia impairs successful defibrillation by altering cardiac electrophysiology.
  • The precise mechanisms underlying ischemia's effect on defibrillation remain unclear.
  • Gap junctions play a critical role in cardiac electrical impulse propagation.

Purpose of the Study:

  • To investigate if regional gap junction inhibition increases biphasic shock defibrillation thresholds (DFT).
  • To determine the impact of gap junction inhibition on myocardial conduction velocity (CV) and effective refractory period (ERP).

Main Methods:

  • Regional heptanol (gap junction inhibitor) or saline was infused into the left anterior descending (LAD) artery of swine.
  • Defibrillation thresholds (DFT) and effective refractory periods (ERP) were measured at multiple myocardial sites.

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  • Regional conduction velocity (CV) was assessed in drug-perfused and non-perfused areas.

    • Main Results:

    • Regional heptanol infusion significantly increased DFT by 33% (P=0.01).
    • Heptanol slowed CV by 42-59% (P<0.01) and increased CV dispersion by 270% (P<0.05) without affecting ERP.
    • Regional heptanol induced spontaneous ventricular fibrillation in all treated animals.

    Conclusions:

    • Impairing regional gap junction conductance increases DFT, suggesting a role in defibrillation failure.
    • Increased conduction velocity dispersion, not altered ERP, is a key mechanism by which gap junction inhibition affects defibrillation efficacy during ischemia.