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Changes in cardiac contractile function and myocardial.

Z F Xia1, P Zhao, J W Horton

  • 1Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9160, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|March 15, 2001
PubMed
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Cutaneous burn trauma significantly impairs cardiac function by increasing intracellular calcium levels in heart cells. This study reveals a direct link between burn-induced calcium dysregulation and postburn cardiac dysfunction.

Area of Science:

  • Cardiology
  • Biochemistry
  • Physiology

Background:

  • Cutaneous burn trauma is known to cause cardiac contraction and relaxation defects.
  • The precise mechanisms underlying postburn cardiac dysfunction remain unclear.
  • Previous research suggests altered myocyte calcium handling is a key factor.

Purpose of the Study:

  • To investigate the correlation between changes in cytosolic free calcium concentration ([Ca(2+)](i)) and cardiac function after burn trauma.
  • To elucidate the role of calcium in burn-related cardiac dysfunction.

Main Methods:

  • Utilized a high dissociation constant (K(d)) calcium indicator, TF-BAPTA, and (19)F NMR spectroscopy.
  • Assessed Left Ventricular Developed Pressure (LVDP) in isolated rat hearts using the Langendorff method.

Related Experiment Videos

  • Performed (31)P and (19)F NMR spectroscopy before and after TF-BAPTA loading.

    • Main Results:

    • Hearts from burned rats exhibited significantly reduced LVDP (<40% of sham burn rats).
    • Burn trauma led to a fourfold increase in cytosolic free calcium concentration ([Ca(2+)](i)).
    • TF-BAPTA loading transiently decreased LVDP by 15%, indicating calcium's role.

    Conclusions:

    • Burn trauma impairs cardiac contractility.
    • This functional defect is directly paralleled by a significant rise in intracellular calcium concentration ([Ca(2+)](i)) in the heart.
    • Altered calcium handling is a critical mechanism in postburn cardiac dysfunction.