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Related Experiment Videos

Persistence of gap junction communication during myocardial ischemia.

M Ruiz-Meana1, D Garcia-Dorado, S Lane

  • 1Department of Cardiology, Hospital General Vall d'Hebron, Barcelona 08035, Spain.

American Journal of Physiology. Heart and Circulatory Physiology
|May 18, 2001
PubMed
Summary

Gap junctions allow rigor to spread between heart cells during ischemia. This cell-to-cell communication persists even after rigor develops, despite changes in acidity and calcium levels.

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Area of Science:

  • Cardiovascular Physiology
  • Cellular Electrophysiology
  • Myocardial Ischemia Research

Background:

  • Myocardial ischemia causes ATP depletion, leading to rigor contracture and increased intracellular calcium ([Ca2+]i).
  • Gap junctions (GJs) mediate electrical coupling between cardiomyocytes, but their function is impaired during ischemia.

Purpose of the Study:

  • To determine if gap junction-mediated chemical coupling facilitates rigor propagation in cardiomyocytes.
  • To assess the persistence of GJ communication after rigor development during ischemia.

Main Methods:

  • Simulated ischemia applied to end-to-end connected and non-connected adult rat cardiomyocyte pairs.
  • Measurement of rigor onset intervals and intracellular calcium ([Ca2+]i) rise.
  • Pharmacological inhibition of GJ with 18alpha-glycyrrhetinic acid.

Related Experiment Videos

  • Assessment of GJ permeability using Lucifer yellow transfer in vitro and in isolated rat hearts.
  • Main Results:

    • Rigor onset was significantly faster (3.7 s) in connected cells compared to non-connected cells (71 s), with similar [Ca2+]i rise.
    • GJ blockade prolonged rigor onset intervals and increased [Ca2+]i differences between connected cells.
    • GJ permeability was detected 10-30 minutes after rigor onset but was lost after 2 hours of ischemia.

    Conclusions:

    • Gap junction-mediated communication enables the propagation of rigor between cardiomyocytes during ischemia.
    • This GJ-mediated rigor propagation persists after rigor development, even with acidosis and elevated [Ca2+]i.
    • GJ function is compromised later in ischemic conditions (after 2 hours).