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Heat stress attenuates ATP-depletion and pH-decrease during cardioplegic arrest.

Sebastian Vogt1, Dirk Troitzsch, Hashim Abdul-Khaliq

  • 1Biomedical Research Center, Cardiovascular Research Lab and Heart Surgery, University Hospital, Philipps-University Marburg, Marburg, Germany. vogts@med.uni-marburg.de

The Journal of Surgical Research
|March 6, 2007
PubMed
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Heat stress pretreatment improves heart function and energy metabolism after prolonged cold ischemia by inducing heat shock proteins (HSPs). This protective effect preserves high-energy phosphates and attenuates pH decrease during ischemia and reperfusion.

Area of Science:

  • Cardiology
  • Biochemistry
  • Physiology

Background:

  • Heat stress induction is known to enhance myocardial tolerance against ischemia.
  • This study investigates cardiac energy metabolism following heat shock protein (HSP) induction in neonatal rabbit hearts subjected to prolonged cold cardioplegic ischemia.

Purpose of the Study:

  • To evaluate the impact of heat stress-induced HSP expression on cardiac energy metabolism and functional recovery after prolonged cold cardioplegic ischemia.
  • To assess the preservation of high-energy phosphates and myocardial pH during ischemia and reperfusion.

Main Methods:

  • Neonatal rabbit hearts were subjected to 2-hour cold cardioplegic ischemia.
  • Heat shock was induced by raising rectal temperature to 42.0-42.5°C for 15 minutes prior to ischemia.

Related Experiment Videos

  • Left ventricular function recovery was measured using aortic flow, cardiac output, and max dP/dt.
  • High-energy phosphate levels were analyzed using 31P-nuclear magnetic resonance spectroscopy.
  • Main Results:

    • Heat stress pretreatment led to significant improvements in left ventricular function (aortic flow, cardiac output, max dP/dt) post-reperfusion compared to controls (P < 0.05).
    • Myocardial energy metabolism was better preserved in heat-stressed hearts, evidenced by increased gamma-ATP, alpha-ATP, beta-ATP, and phosphocreatine levels.
    • The reduction in myocardial pH during ischemia was attenuated in the heat-stressed group.

    Conclusions:

    • Heat stress pretreatment confers beneficial effects on functional myocardial recovery and energy metabolism following prolonged cold cardioplegic ischemia.
    • The observed protective effects suggest a role for heat shock proteins in preserving mitochondrial membrane potential and attenuating ischemic damage.