Glucose-induced decrease in glutamate levels in ischemic human brain by in-vivo microdialysis.
Glutamate is one of the principal neurotoxins in the pathogenesis of ischemic neuronal injury. Elevated glutamate levels in ischemia have been well documented in many animal stroke models. Recent work in humans also shows a similar trend. We have used our acute focal ischemic model of the human brain to study the response of glutamate levels by in vivo microdialysis during ischemia using two different perfusates. The addition of 30 mM of glucose to the perfusate attenuated the percentages of dialysate glutamate levels from 4.27 +/- 1.7 to 1.34 +/- 0.47 (P < 0.001) during partial ischemia and from 21.42 +/- 6.05 to 7.25 +/- 1.43 (P < 0.05) with total ischemia. The pre-ischemic values of glutamate were similar with the two perfusates. These results indicate that the ischemia-induced rise in glutamate is attenuated by exogenous glucose delivery in the human stroke model.
Kanthan
R
R
Department of Medicine (Neurology), Saskatchewan Stroke Research Centre, College of Medicine, Saskatoon, Canada.
Shuaib
A
A
Griebel
R
R
Miyashita
H
H
Kalra
J
J
D000596:Amino Acids / Q000032:analysis / Q000378:metabolism; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology*; D002545:Brain Ischemia / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D005947:Glucose / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism*; D006801:Humans; D017551:Microdialysis
D000596:Amino Acids; D018698:Glutamic Acid; D005947:Glucose