SUMMARY Whether the calcium entry blocker, nimodipine, prevents the increase in the concentration of free fatty adds and metabolic disturbances during ischemia and promotes functional and metabolic recovery after reclrculation 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 preischemk 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.
Stroke Vol 17, No 3, 1986RECENTLY, considerable interest has been centered on the role of calcium in irreversible ischemic brain damage. 1 2 Ischemic depolarization of cell membrane is associated with a precipitous influx of calcium from the extracellular to the intracellular compartment, and, as a consequence, intracellular calcium increase. 3 The elevated cytosolic calcium induces impairment of the mitochondrial function that leads to failure of ATP production and induces activation of Ca 2+ -ATPase resulting in a further reduction of ATP.