• Nariyuki Hayashi
  • Dalton W. Dietrich


In addition to slowing oxygen consumption [5], posttraumatic and ischemic hypothermia has been reported to blunt the rise in extracellular levels of excitatory amino acids after parasagittal F-P injury [1, 2, 3]. However, in a model of controlled cortical impact, hypothermia failed to attenuate the rise in extracellular aspartate and glutamate although contusion volume was significantly reduced by cooling [4]. In a model of spinal cord ischemia, hypothermia effectively attenuated extracellular glutamate release [6]. Wakamatsu and colleagues [8] reported that intraischemic moderate hypothermia (32°C) significantly reduced glutamate concentrations of intrathecal dialysate and improved neurologic status and histopathology after spinal cord ischemia. In contrast, other reports have indicated that hypothermia did not attenuate extracellular accumulation of excitatory amino acids or improve energy metabolism. For example, hyperthermia (39°C) during middle cerebral artery occlusion led to increased levels of extracellular glutamate compared to normothermic animals [7].


Middle Cerebral Artery Occlusion Excitatory Amino Acid Therapeutic Hypothermia Glutamate Concentration Spinal Cord Ischemia 
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Copyright information

© Springer Japan 2004

Authors and Affiliations

  • Nariyuki Hayashi
    • 1
    • 2
  • Dalton W. Dietrich
    • 3
    • 4
  1. 1.Nihon University Emergency Medical CenterTokyoJapan
  2. 2.Department of Emergency and Critical Care MedicineNihon University School of MedicineTokyoJapan
  3. 3.Department of Neurological Surgery, Neurology and Cell Biology and AnatomyUniversity of Miami School of MedicineMiamiUSA
  4. 4.The Miami Project to Cure ParalysisMiamiUSA

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