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Related Experiment Videos

Gap junction uncoupling protects the heart against ischemia.

Adam E Saltman1, Tunc O Aksehirli, Virginijus Valiunas

  • 1Division of Cardiothoracic Surgery, The Institute for Molecular Cardiology, State University of New York at Stony Brook, Health Sciences Center T19-080, Stony Brook, NY 11794-8191, USA. adam.saltman@sunysb.edu

The Journal of Thoracic and Cardiovascular Surgery
|August 9, 2002
PubMed
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Blocking gap junctions before heart ischemia significantly reduces heart muscle damage. This protective effect does not involve the adenosine triphosphate-dependent potassium channel.

Area of Science:

  • Cardiovascular Physiology
  • Myocardial Protection
  • Cellular Signaling

Background:

  • Myocardial protection against ischemia can be achieved through various stimuli.
  • Investigated the potential cardioprotective role of gap junction uncoupling prior to ischemic events.
  • Explored the involvement of the adenosine triphosphate-dependent potassium channel in pharmacologic preconditioning and its relation to gap junction physiology.

Purpose of the Study:

  • To determine if uncoupling gap junctions before ischemia confers myocardial protection.
  • To elucidate the role of the adenosine triphosphate-dependent potassium channel in this protective mechanism.

Main Methods:

  • Rabbit hearts were perfused using a Langendorff apparatus.
  • Groups received heptanol (gap junction uncoupler), 2,3-butanedione monoxime (electromechanical uncoupler), or no drug.

Related Experiment Videos

  • Left anterior descending coronary artery occlusion followed by reperfusion was performed.
  • Measurements included action potential duration, left ventricular developed pressure, coronary flow, and infarct size.

    • Main Results:

    • Heptanol significantly reduced infarct size (46% to 22%).
    • 2,3-butanedione monoxime did not significantly reduce infarct size.
    • Glybenclamide did not prevent the infarct-reducing effect of heptanol.
    • No significant differences in developed pressure or action potential duration were observed between groups.

    Conclusions:

    • Directly blocking gap junctions provides myocardial preconditioning.
    • This protection is independent of reduced developed pressure before ischemia.
    • The mechanism does not involve the adenosine triphosphate-dependent potassium channel.