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To evaluate the direct effects of a barbiturate on cerebral functions without its influence on brain perfusion pressure, circulatory hormones and metabolites, the electroencephalogram (EEG) was studied in the isolated rat head. Male Wistar rats were anesthetized, and EEG electrodes were inserted into the cranium. A Krebs-Ringer bicarbonate buffer solution containing heparinized rat whole blood, 20 mmol/l glucose, 200 mmol/l mannitol and 0.1 mg/ml dexamethasone was used for the perfusate. The bilateral common carotid arteries were cannulated, pumped at a rate of 6 ml/min and the head was isolated. The venous effluent was reoxygenated and recirculated into the brain. Twenty-five min after isolation of the heads pentobarbital was added to the perfusate at concentrations of 0.1, 0.5 and 2.5 mg/ml. EEG was recorded before and during perfusion. EEG activity could be recorded for more than 25 min after the beginning of perfusion. EEG activity gradually declined from 42+/-5 microV before perfusion (in vivo) to 4+/-1 microV at 25 min after the beginning of perfusion. Then, 3 min after the addition of pentobarbital, the EEG activity became significantly higher in the high dose groups; 12+/-3 microV in the 0.5 mg/ml group (p<0.05) and 12+/-1 microV in 2.5 mg/ml group (p<0.05) compared with the group without pentobarbital (2+/-2 microV). The present study suggests that a barbiturate has mitigating effects on the brain damage induced by the in vitro brain perfusion.