Advertisement

Excitotoxicity

  • Nariyuki Hayashi
  • Dalton W. Dietrich

Abstract

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].

Keywords

Middle Cerebral Artery Occlusion Excitatory Amino Acid Therapeutic Hypothermia Glutamate Concentration Spinal Cord Ischemia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Globus MY-T, Alonso O, Dietrich WD, Busto R, Ginsberg MD (1995) Glutamate release and free radical production following brain injury: effects of posttraumatic hypothermia. J Neurotrauma 65:1704–1711Google Scholar
  2. 2.
    Globus MY-T, Busto R, Lin B, Schnippering H, Ginsberg MD (1995) Detection of free radical activity during transient global ischemia and recirculation: effects of intraischemic brain temperature modulation. J Neurochem 65:1250–1256PubMedCrossRefGoogle Scholar
  3. 3.
    Goss JR, Styren SD, Miller PD, Kochanek PM, Palmer AM, Graenen G, Jeftinija S, Grants I, Lucas JH (1996) The role of excitatory amino acids in hypothermic injury to mammalian spinal cord neurons. J Neurotrauma 13:809–818CrossRefGoogle Scholar
  4. 4.
    Palmer AM, Marion DW, Botsceller ML, Redd EE (1993) Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury-induced elevations in interstitial concentrations of aspartate and glutamate. J Neurotrauma 10:363–372PubMedCrossRefGoogle Scholar
  5. 5.
    Rosomoff HL, Holaday S (1954) Cerebral blood flow and cerebral oxygen consumption during hypothermia. Am J Physiol 179:85–88PubMedGoogle Scholar
  6. 6.
    Saganova K, Marsala M (1994) Intrathecal administration of dizocilpine maleate (MK-801) attenuates ischemic damage in the rabbit spinal cord. Exp Neurol 130:337–343PubMedCrossRefGoogle Scholar
  7. 7.
    Tagaki K, Ginsberg MD, Globus MY-T, Martinez E, Busto R (1994) Effect of hyperthermia on glutamate release in ischemic penumbra after middle cerebral artery occlusion in rats. Am Physiol Soc H1770–H1775Google Scholar
  8. 8.
    Wakamatsu H, Matsumoto M, Nakakimura K, Sakabe T (1999) The effects of moderate hypothermia and intrathecal tetracaine on glutamate concentrations of intrathecal dialysate and neurologic and histopathologic outcome in transient spinal cord ischemia in rabbits. Anesth Analg 88:56–62PubMedGoogle Scholar

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

Personalised recommendations