Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.
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.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001921:Brain / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis / Q000187:drug effects; D006943:Hyperglycemia / Q000150:complications* / Q000503:physiopathology; D007328:Insulin / Q000494:pharmacology*; D002546:Ischemic Attack, Transient / Q000150:complications / Q000503:physiopathology*; D007700:Kinetics; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D007328:Insulin; D005947:Glucose