Effect of acute alcohol on ischemia-induced glutamate release and brain damage

Epidemiological studies show that chronic ethanol consumption at high doses enhances the risk of cerebral stroke. The mechanisms responsible for the g reater vulnerability of alcoholics' brains to stroke have to be completely understood, but a role for excitatory amino acids has been suggested. In or der to study the interaction between alcohol and ischemia, we investigated the effect of acute alcohol administration in a model of focal cerebral isc hemia. In particular, we evaluated the release of glutamate and aspartate f rom the cerebral frontal cortex by a transdialysis technique. Alcohol was a cutely administered at 1.5 and 3.0 g/kg ip. During the period of maximal al coholemia, ethanol almost abolished the ischemia-induced release of glutama te leading to glutamate values around or below the basal. Aspartate levels were unaltered both following ischemia and alcohol + ischemia. The decrease in glutamate release, however, was not accompanied by a significant reduct ion of the extension of the damaged area assessed by histological analysis. (C) 2001 Elsevier Science Inc. All rights reserved.