Calcium channel blockers correct acidosis in ischemic rat brain without altering cerebral blood flow

We compared the effects of intravenous infusions of 40 micrograms/kg/min verapamil (n = 5), 0.5 microgram/kg/min nimodipine (n = 5), and 5 ng/kg/min prostacyclin (n = 6) and no treatment (n = 6) on local cerebral pH and local cerebral blood flow in middle cerebral artery-occluded rats 90 minutes after the ischemic insult. Local cerebral pH and local cerebral blood flow were determined simultaneously by a double-label autoradiographic technique. The infusions were started 15 minutes after completion of the occlusion and ended at decapitation 90 minutes after completion of the occlusion. Cortical pH for four regions in the ischemic middle cerebral artery territory of rats receiving verapamil or nimodipine was normalized (mean +/- SEM 6.90 +/- 0.02 and 7.01 +/- 0.01, respectively, for the parietal, sensorimotor, frontal, and auditory cortexes), while mean +/- SEM pH in rats receiving prostacyclin was 6.79 +/- 0.01; in untreated rats, mean +/- SEM pH in the same brain regions was 6.72 +/- 0.01. Local cerebral pH in the verapamil- or nimodipine-treated rats was thus significantly different from that in untreated rats (p less than 0.05). Local cerebral blood flow in treated rats was not different from that in untreated ones. Our findings suggest that calcium channel blockers correct ischemic cerebral acidosis by metabolic mechanisms rather than by changes in blood flow.