Whether the calcium entry blocker, nimodipine, prevents the increase in the concentration of free fatty acids and metabolic disturbances during ischemia and promotes functional and metabolic recovery after recirculation were examined. Severe forebrain ischemia in rats was induced by four-vessel occlusion with mild hypotension. After 30 minutes of ischemia, recirculation was started by removal of the arterial clamps and by increasing blood pressure to the preischemic level. Recovery of EEG activity following recirculation was better in the nimodipine-treated group than in the control group. During the ischemic period, there were no significant differences in accumulation of free fatty acids or in depletion of ATP between treated and control groups. At 120 minutes following recirculation, recovery of the ATP level was significantly better in the treated group than in the control group. Therefore, the promotion of functional and metabolic recovery by nimodipine-treatment is suggested to be not due to the prevention of an accumulation of free fatty acids nor to the depletion of ATP during the ischemic period, but to either improvement of postischemic hypoperfusion or a direct action on metabolic processes during reperfusion period.