The effect of nicardipine on neuronal function following ischemia

In cerebral ischemia, it has been proposed that calcium influx into neurons results in irreversible cellular injury during reperfusion. We administered nicardipine, a dihydropyridine calcium entry blocker, by continuous subcutaneous infusion to twenty five rats beginning before (PR) or following (PO) ischemia, and compared somatosensory evoked potentials (SEPs) to twenty eight ischemic control animals. Comparable ischemic cellular changes were seen in the hippocampi of all animals. SEP amplitude was higher in both the PR (p <.005) and PO (p <.0005) groups compared to controls. This effect was found in all three components (P₁, N₁, P₂) of the evoked response. Plasma nicardipine levels of 6-10 ng/ml were associated with mild hypotension. We conclude that nicardipine improved neuronal function as measured by SEPs when administered before or after ischemia, most likely by interrupting the cytotoxic events occurring in cortical neurons during reperfusion.