Nimodipine shws promise in the prevention and treatment of
brain ischemia. We examined the interaction of
nimodipine pretreatment in a dose sufficient to prevent postischemic hypoperfusion 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 [14C]
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 less than 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 less than 0.05). Although
nimodipine tended to increase rCBF and decrease regional cerebrovascular resistance (rCVR), this was significant only for hemispheric rCVR (p less than 0.05). There was a borderline effect for
nimodipine to increase rCGU, especially during hypocarbia.(ABSTRACT TRUNCATED AT 250 WORDS)