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Calcium preconditioning in human myocardium

B S Cain1, D R Meldrum, X Meng

  • 1Department of Surgery, University of Colorado Health Sciences Center, Denver 80262, USA.

The Annals of Thoracic Surgery
|May 16, 1998
PubMed
Summary
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Calcium (Ca2+) preconditioning protects human heart tissue from damage caused by ischemia-reperfusion injury. This protective effect is dependent on protein kinase C (PKC) signaling pathways.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Ischemic stress and protein kinase C (PKC) receptor stimuli offer cardiac protection against ischemia-reperfusion injury.
  • Exogenous calcium (Ca2+) pretreatment provides PKC-mediated protection in animal models.
  • The efficacy of Ca2+ preconditioning in human myocardium and its underlying PKC mechanism remain unclear.

Purpose of the Study:

  • To investigate whether Ca2+ preconditioning confers postischemic functional protection in human myocardium.
  • To determine if this protection is mediated by a protein kinase C (PKC)-dependent mechanism.

Main Methods:

  • Human atrial trabeculae were subjected to simulated ischemia (45 minutes) and reperfusion (120 minutes).
  • Trabeculae received either exogenous CaCl2 (Ca2+ preconditioning) or vehicle before ischemia.

Related Experiment Videos

  • Protein kinase C (PKC) inhibition was applied concurrently with Ca2+ preconditioning in some groups.
  • Main Results:

    • Ischemia-reperfusion significantly reduced postischemic developed force in human atrial trabeculae.
    • Ca2+ preconditioning significantly protected human myocardium against ischemia-reperfusion injury compared to controls.
    • Inhibition of protein kinase C (PKC) abolished the protective effects of Ca2+ preconditioning.

    Conclusions:

    • Ca2+ preconditioning is a potent strategy for inducing protein kinase C (PKC)-mediated protection in human myocardium.
    • This study demonstrates the clinical relevance of Ca2+ preconditioning for mitigating ischemia-reperfusion injury in humans.