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High energy compound stability during experimental brain death.

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  • 1INSERM EMI-U 0226, Laboratoire de Physiologie, Faculté de médecine Lyon-Nord, 8 avenue Rockefeller, 69373 Lyon Cedex 08, France. ferrera@lyon.inserm.fr

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Sudden brain death (BD) causes a rapid increase in catecholamines and decreased heart contractility. However, myocardial high energy phosphate stores remain unaffected after cardioplegia, suggesting early heart injury during BD is not ischemic.

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Area of Science:

  • Cardiology
  • Physiology
  • Biochemistry

Background:

  • Sudden brain death (BD) can impact myocardial function.
  • Understanding the effects of BD on heart energy stores is crucial for organ preservation.

Purpose of the Study:

  • To investigate the impact of sudden brain death on myocardial function and high energy phosphate (HEP) levels.
  • To determine if early heart injury during BD is an ischemic process.

Main Methods:

  • Brain death was induced in swine via cerebral vessel ligation.
  • Myocardial HEP stores were assessed using (31)P-NMR spectroscopy and HPLC.
  • Left ventricular contractility and intracellular pH were measured.

Main Results:

  • Brain death led to a significant increase in catecholamines and a decrease in left ventricular contractility.
  • No significant differences in HEP compounds (ATP, ADP, AMP, PCr, Pi) or intracellular pH were found between brain death and control groups after cardioplegia.
  • The energetic index and ATP/Pi ratio remained unchanged.

Conclusions:

  • Early heart injury during brain death does not appear to be primarily ischemic.
  • Myocardial high energy phosphate stores are preserved despite the physiological changes induced by brain death.