A pressing clinical question is how acute ethanol exposure might alter the
outcome of a simultaneous transient ischemic attack (TIA), since ethanol is
known to dysregulate key intermediary metabolites post-ischemia. Mongolian
gerbils were administered ethanol (1 or 4g/kg, sc) 1 hour before induction
of transient ischemia, via bilateral carotid occlusions of 5 minutes durat
ion. A control group was administered isotonic saline and rendered ischemic
. All animals were maintained normothermic during the ischemic procedure. S
ubjects underwent behavioral assay of acquisition to the water maze 7 days
after recovery from the surgery, and neuropathological examination 1-month
after the ischemic brain insult. There were no behavioral or neuropathologi
cal between-group differences suggesting that mechanisms other than adverse
ethanol-induced perturbations of ischemic processes predominate in mediati
ng epidemiological findings of elevated stroke morbidity with high ethanol
consumption.