Influence of ethanol on the energy metabolism of ischemic and postischemic brain.
This study documents the effects of an intoxicating dose of ethanol on the energy metabolism and electrophysiological function of rat brain exposed for 0.5 h to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. One-hour exposure to 5 g kg-1 ethanol led to no significant alterations of the preischemic cerebral contents of glucose, lactate, or energy phosphates. Animals receiving ethanol or isovolumetric amounts of 0.9% saline showed statistically equivalent decreases in glucose, ATP, and phosphocreatine and increases in lactate, ADP, and AMP during 0.5 h of ischemia. Upon recirculation for 0.5-24 h, animals receiving ethanol again showed no significant differences from saline-treated animals in the rate of return of glucose, lactate, and energy metabolites to control levels. Animals receiving ethanol showed a trend for a faster and more complete normalization of the EEG during recirculation. It is concluded that under controlled experimental conditions, intoxicating doses of ethanol have no detrimental effect on the energy metabolism of ischemic and postischemic brain.
MacMillan
V
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Department of Medicine, University of Toronto, Ontario, Canada.
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001786:Blood Glucose / Q000032:analysis; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000378:metabolism*; D004569:Electroencephalography; D004734:Energy Metabolism / Q000187:drug effects*; D000431:Ethanol / Q000097:blood / Q000378:metabolism / Q000494:pharmacology*; D005947:Glucose / Q000134:cerebrospinal fluid / Q000378:metabolism; D007773:Lactates / Q000097:blood / Q000134:cerebrospinal fluid / Q000378:metabolism; D019344:Lactic Acid
D001786:Blood Glucose; D007773:Lactates; D019344:Lactic Acid; D000431:Ethanol; D005947:Glucose