The glucose paradox in cerebral ischemia. New insights.
The present in vivo findings that lactate, accumulated during an ischemic episode, is an essential aerobic energy substrate during the initial postischemic period are in full agreement with out in vitro findings. Moreover, the beneficial effects of hyperglycemia are also in agreement with our and others' in vitro results that have demonstrated a neuroprotective effect of glucose against hypoxic change. The aggravation of ischemic delayed neuronal damage by glucose loading 15 min prior to the ischemic insult is likely the result of glucose induction of a short-acting (30 to 60 min) systemic factor (hormonal?) that, when combined with an ischemic insult, potentiates the ischemic damage.
Schurr
A
A
Department of Anesthesiology, University of Louisville, School of Medicine, Kentucky 40292, USA. A0schu01@ulkyvm.louisville.edu
Payne
R S
RS
Tseng
M T
MT
Miller
J J
JJ
Rigor
B M
BM
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006323:Heart Arrest; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology*; D006943:Hyperglycemia / Q000503:physiopathology; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000473:pathology*; D007773:Lactates / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D001786:Blood Glucose; D007773:Lactates; D005947:Glucose