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Glucose-induced decrease in glutamate levels in ischemic human brain by in-vivo microdialysis

R Kanthan1, A Shuaib, R Griebel

  • 1Department of Medicine (Neurology), Saskatchewan Stroke Research Centre, College of Medicine, Saskatoon, Canada.

Neuroscience Letters
|May 17, 1996
PubMed
Summary
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Exogenous glucose delivery attenuated ischemia-induced glutamate rise in a human stroke model. This finding suggests glucose may mitigate neurotoxicity during ischemic events.

Area of Science:

  • Neuroscience
  • Ischemic Stroke Pathophysiology

Background:

  • Glutamate is a key neurotoxin in ischemic neuronal injury.
  • Elevated glutamate levels during ischemia are documented in animal models and increasingly in humans.

Purpose of the Study:

  • To investigate the effect of exogenous glucose on glutamate levels during acute focal ischemia in a human brain model.
  • To determine if glucose administration can attenuate the rise in extracellular glutamate during ischemic conditions.

Main Methods:

  • Utilized an acute focal ischemic model of the human brain.
  • Employed in vivo microdialysis to measure glutamate levels during ischemia.
  • Compared glutamate levels using two perfusates: one with 30 mM glucose and a control.

Main Results:

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  • The addition of 30 mM glucose to the perfusate significantly attenuated the percentage increase in dialysate glutamate levels during both partial (4.27% to 1.34%) and total ischemia (21.42% to 7.25%).
  • Pre-ischemic glutamate levels were similar between the two perfusate groups, indicating the observed attenuation was specific to the ischemic period.

Conclusions:

  • Exogenous glucose delivery effectively attenuates the ischemia-induced rise in extracellular glutamate in a human stroke model.
  • These findings suggest that glucose administration may be a potential therapeutic strategy to reduce glutamate-mediated neurotoxicity in stroke patients.