Effect of Nimodipine on Cerebral Blood Flow and Metabolism in Rats During

Nimodipine shows promise in the prevention and treatment of brain ischemia. We examined the interaction of nimodipine pretreatment in a dose sufficient to prevent postischemic hypoperfu-sion and hyperventilation. We studied four groups of rats: normocarbia plus vehicle (Group 1, n=5), hypocarbia plus vehicle (Group 2, n=4), normocarbia plus nimodipine (Group 3, n=7), and hypocarbia plus nimodipine (Group 4, n=6). Groups 3 and 4 received 1 mg/kg i.p. nimodipine, and Groups 1 and 2 received an equivalent amount of vehicle. Ventilation was left unaltered in Groups 1 and 3 or increased to lower Paco2 to 21-24 mm Hg in Groups 2 and 4. Determination of regional cerebral glucose utilization (rCGU) was carried out using the [3H]2-deoxyglucose method, and regional cerebral blood flow (rCBF) was determined by the indicator fractionation method using [l4C]iodoantipyrine. The brain regions studied were the cerebral hemispheres, the diencephalon, the cerebellum, and the brainstem. Hyperventilation in Groups 2 and 4 from approximately 38 to 22 mm Hg reduced rCBF to 60 % of normocarbic levels (p<0.05). The slope and intercept of this response were similar in vehicle- and nimodipine-pretreated rats. Nimodipine modestly decreased mean arterial blood pressure by 20 % and increased plasma glucose concentration by 60 % (p<0.05). Although nimodipin