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
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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