To study the protective effect of phenytoin on postischemic brain damage, total cerebral ischemia was produced for 8-12 min (aortic occlusion balloon catheter method) in 36 adult mongrel dogs. The regional cerebral blood flow (rCBF), sodium:potassium ratio in the cerebral cortex, electroencephalogram (EEG), and plasma electrolytes in the superior sagittal sinus blood were examined before ischemia and during the acute stage up to 120 min after recirculation in the control and phenytoin-treated groups. Measurement of rCBF (microsphere method) indicated easing of postischemic hypoperfusion of the cerebral cortex. The time from total cerebral ischemia to EEG electrical silence was significantly prolonged, and recovery of the electrical activity after recirculation was hastened. The increase in plasma potassium concentration in the superior sagittal sinus tended to be suppressed immediately after recirculation, and the sodium:potassium ratio in the cerebral cortex was lowered. Phenytoin increased the rCBF in the cerebral cortex, hastened the recovery of electrical activity, and stabilized the water and electrolyte balance in the cerebral cortex, suggesting some protecting effect on total cerebral ischemia.