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Hemispheric ischemia was induced in normothermic, artificially ventilated and anesthetized rats, by electrocauterization of the vertebral arteries and a transient occlusion of the common carotid arteries for 10 minutes. Cerebrospinal fluid (CSF) was continuously pumped out of the third cerebral ventricle for potassium, dopamine and serotonin metabolite determinations. Levels were stable until ischemia, which interrupted the CSF production. During early recirculation a marked increase in dopamine metabolites occurred. The metabolite of serotonin increased slightly with a delay. Potassium in CSF was transitorily increased following ischemia. Reserpine pretreatment prevented most of the changes such as the early increase in dopamine metabolites. A delayed increase of these metabolites was still observed. This model of short ischemia altered the neurological functioning and survival time of the animals especially 15 minutes after removal of bilateral carotid occlusion, as compared to the later periods of observation. This model is therefore applicable to the study of cerebral alterations secondary to ischemia in vivo. The presently observed alterations of metabolite levels could reflect an increased neuronal release of parents monoamines that could participate to the neurological deficit.