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Updated: Jun 3, 2026

A Modified Simple Method for Induction of Myocardial Infarction in Mice
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A Modified Simple Method for Induction of Myocardial Infarction in Mice

Published on: December 3, 2021

Increased Cell-Cell Coupling Increases Infarct Size and Does not Decrease Incidence of Ventricular Tachycardia in

Kevin A Prestia1, Eugene A Sosunov, Evgeny P Anyukhovsky

  • 1Department of Pharmacology, College of Physicians and Surgeons, Columbia University New York, NY, USA.

Frontiers in Physiology
|March 23, 2011
PubMed
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This summary is machine-generated.

Enhancing cardiac cell-cell communication by increasing connexin32 (Cx32) expression did not prevent ventricular tachycardia (VT) but unexpectedly increased heart attack size in mice.

Area of Science:

  • Cardiovascular Research
  • Molecular Cardiology
  • Arrhythmia Mechanisms

Background:

  • Connexin43 (Cx43) gap junctional conductance is explored for antiarrhythmic effects.
  • Concerns exist that gap junction molecule transmission may enlarge infarct size.
  • The role of sustained gap junction channel opening in cardiac ischemia is unclear.

Purpose of the Study:

  • To investigate if maintaining open gap junction channels impacts infarct size.
  • To determine if open gap junction channels affect ventricular tachycardia (VT) induction post-coronary occlusion.
  • To assess the impact of expressing connexin32 (Cx32), a pH- and voltage-independent connexin isoform, on cardiac outcomes.

Main Methods:

  • Adenovirus-mediated Cx32 expression was induced in wild-type (WT) mouse ventricles (Cx32inj).
Keywords:
antiarrhythmic therapyconnexin32connexin43coronary occlusioninfarct sizemyocardial infarction

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  • Coronary occlusion was performed to induce myocardial infarction and VT.
  • Infarct size and VT inducibility via programmed electrical stimulation were quantified.

    • Main Results:

    • Cx32inj hearts exhibited significantly larger infarct sizes compared to WT controls (44.3% vs. 22.9%).
    • No significant difference in VT inducibility was observed between Cx32inj and WT mice (50% vs. 55%).
    • Increased cell-cell communication via Cx32 did not provide antiarrhythmic benefits.

    Conclusions:

    • Augmenting cell-cell communication by increasing Cx32 expression exacerbates infarct size following coronary occlusion.
    • Enhanced gap junction activity does not reduce VT inducibility in this model.
    • The proposed antiarrhythmic strategy of increasing gap junctional conductance may have detrimental effects on infarct size.