Hypothermia Ameliorates Ischemic Brain Damage and Suppresses the Release of Extracellular Amino Acids in both Normo- and Hyperglycemic Subjects

Hypothermia Ameliorates Ischemic Brain Damage and Suppresses the Release of Extracellular Amino... It has previously been shown that hypothermia markedly reduces cellular release of the excitatory amino acid glutamate and ameliorates ischemic damage. Based on extensive data showing that preischemic hyperglycemia exaggerates brain damage due to transient forebrain ischemia we posed the question whether glutamate release during ischemia in hyperglycemic rats is attenuated or prevented by induced hypothermia, and if such attenuation/prevention correlates with amelioration of the characteristic brain damage observed in hyperglycemic subjects. The experiments were performed in rats subjected to a 15-min period of forebrain ischemia, plasma glucose concentration being maintained at ∼5 mM (control) or ∼20 mM (hyperglycemia) prior to ischemia. Extracellular amino acid concentrations were measured by HPLC techniques on microdialysis samples which were collected from left dorsal hippocampus and right neocortex, and tissue damage was assessed by histopathology. Hypothermia (30°C), which was induced 45 min prior to ischemia, reduced the neuronal damage not only in the ischemia-vulnerable regions but also in the normally ischemia-resistant areas that are recruited in the damage process in hyperglycemic subjects. The extracellular glutamate concentration was markedly increased in response to the ischemic insult in normothermic–normoglycemic animals. The concentration of glutamate was further increased in normothermic–hyperglycemic animals. Hypothermia inhibited the rise in glutamate concentrations, as well as in the concentrations of other excitatory and inhibitory amino acids. It is discussed whether hypothermia reduces the hyperglycemia-mediated damage by inhibiting extracellular glutamate release during an ischemic transient. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Neurology Elsevier

Hypothermia Ameliorates Ischemic Brain Damage and Suppresses the Release of Extracellular Amino Acids in both Normo- and Hyperglycemic Subjects

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Publisher
Elsevier
Copyright
Copyright © 1999 Academic Press
ISSN
0014-4886
D.O.I.
10.1006/exnr.1999.7088
Publisher site
See Article on Publisher Site

Abstract

It has previously been shown that hypothermia markedly reduces cellular release of the excitatory amino acid glutamate and ameliorates ischemic damage. Based on extensive data showing that preischemic hyperglycemia exaggerates brain damage due to transient forebrain ischemia we posed the question whether glutamate release during ischemia in hyperglycemic rats is attenuated or prevented by induced hypothermia, and if such attenuation/prevention correlates with amelioration of the characteristic brain damage observed in hyperglycemic subjects. The experiments were performed in rats subjected to a 15-min period of forebrain ischemia, plasma glucose concentration being maintained at ∼5 mM (control) or ∼20 mM (hyperglycemia) prior to ischemia. Extracellular amino acid concentrations were measured by HPLC techniques on microdialysis samples which were collected from left dorsal hippocampus and right neocortex, and tissue damage was assessed by histopathology. Hypothermia (30°C), which was induced 45 min prior to ischemia, reduced the neuronal damage not only in the ischemia-vulnerable regions but also in the normally ischemia-resistant areas that are recruited in the damage process in hyperglycemic subjects. The extracellular glutamate concentration was markedly increased in response to the ischemic insult in normothermic–normoglycemic animals. The concentration of glutamate was further increased in normothermic–hyperglycemic animals. Hypothermia inhibited the rise in glutamate concentrations, as well as in the concentrations of other excitatory and inhibitory amino acids. It is discussed whether hypothermia reduces the hyperglycemia-mediated damage by inhibiting extracellular glutamate release during an ischemic transient.

Journal

Experimental NeurologyElsevier

Published: Jul 1, 1999

References

  • Excitotoxic cell death
    Choi, D.W.
  • Glutamate-treated rat cortical neuronal cultures die in a way different from the classical apoptosis induced by staurosporine
    MacManus, J.P.; Rasquinha, I.; Black, M.A.; Laferriere, N.B.; Monette, R.; Walker, T.; Morley, P.
  • Role of endogenous taurine on the glutamate analogue-induced neurotoxicity in the rat hippocampus in vivo
    Menéndez, N.; Solı́s, J.M.; Herreras, O.; Herranz, A.S.; Martı́n, D.R.
  • Calcium-mediated mechanisms of ischemic injury and protection
    Morley, P.; Hogan, M.J.; Hakim, A.M.
  • Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model
    Smith, M.-L.; Bendek, G.; Dahlgren, N.; Rosén, I.; Wieloch, T.; Siesjö, B.K.
  • Astrocyte metabolism of ( 15 N)glutamine: Implications for the glutamine–glutamate cycle
    Yudkoff, M.; Nissim, I.; Pleasure, D.

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