Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.

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Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate. / Siemkowicz, E; Hansen, A J; Gjedde, A.

In: Brain Research, Vol. 243, No. 2, 1982, p. 386-90.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Siemkowicz, E, Hansen, AJ & Gjedde, A 1982, 'Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.', Brain Research, vol. 243, no. 2, pp. 386-90.

APA

Siemkowicz, E., Hansen, A. J., & Gjedde, A. (1982). Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate. Brain Research, 243(2), 386-90.

Vancouver

Siemkowicz E, Hansen AJ, Gjedde A. Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate. Brain Research. 1982;243(2):386-90.

Author

Siemkowicz, E ; Hansen, A J ; Gjedde, A. / Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate. In: Brain Research. 1982 ; Vol. 243, No. 2. pp. 386-90.

Bibtex

@article{2da55a70b31511debc73000ea68e967b,
title = "Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.",
abstract = "To identify the mechanism by which hyperglycemia impairs recovery after cerebral ischemia, cortical blood flow (CBF), cortical metabolic rate for oxygen (CMRO2), and the cortical phosphorylation rate for glucose (CPRg1c) were measured in rats 1 h after a global ischemic insult of the brain. A control group remained hyperglycemic after ischemia. The experimental group received insulin which reduced plasma glucose during the period of recirculation after ischemia. Thus, the brains of both groups were hyperglycemic before and during ischemia. The CMRO2 after ischemia was higher in insulin-treated rats than in hyperglycemic rats (250 vs 168 mumol . 100 g-1 . min-1) while the CPRg1c was lower (22 vs 58 mumol . 100 g-1 . min-1). We conclude that glucose-induced inhibition of oxygen consumption in brain contributes to the impaired recovery after ischemia.",
author = "E Siemkowicz and Hansen, {A J} and A Gjedde",
year = "1982",
language = "English",
volume = "243",
pages = "386--90",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.

AU - Siemkowicz, E

AU - Hansen, A J

AU - Gjedde, A

PY - 1982

Y1 - 1982

N2 - To identify the mechanism by which hyperglycemia impairs recovery after cerebral ischemia, cortical blood flow (CBF), cortical metabolic rate for oxygen (CMRO2), and the cortical phosphorylation rate for glucose (CPRg1c) were measured in rats 1 h after a global ischemic insult of the brain. A control group remained hyperglycemic after ischemia. The experimental group received insulin which reduced plasma glucose during the period of recirculation after ischemia. Thus, the brains of both groups were hyperglycemic before and during ischemia. The CMRO2 after ischemia was higher in insulin-treated rats than in hyperglycemic rats (250 vs 168 mumol . 100 g-1 . min-1) while the CPRg1c was lower (22 vs 58 mumol . 100 g-1 . min-1). We conclude that glucose-induced inhibition of oxygen consumption in brain contributes to the impaired recovery after ischemia.

AB - To identify the mechanism by which hyperglycemia impairs recovery after cerebral ischemia, cortical blood flow (CBF), cortical metabolic rate for oxygen (CMRO2), and the cortical phosphorylation rate for glucose (CPRg1c) were measured in rats 1 h after a global ischemic insult of the brain. A control group remained hyperglycemic after ischemia. The experimental group received insulin which reduced plasma glucose during the period of recirculation after ischemia. Thus, the brains of both groups were hyperglycemic before and during ischemia. The CMRO2 after ischemia was higher in insulin-treated rats than in hyperglycemic rats (250 vs 168 mumol . 100 g-1 . min-1) while the CPRg1c was lower (22 vs 58 mumol . 100 g-1 . min-1). We conclude that glucose-induced inhibition of oxygen consumption in brain contributes to the impaired recovery after ischemia.

M3 - Journal article

C2 - 7049325

VL - 243

SP - 386

EP - 390

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -

ID: 14945624