Stroke, Vol 17, 213-219, Copyright © 1986 by American Heart Association
J Grotta, J Spydell, C Pettigrew, P Ostrow and D Hunter
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 less than .005) and PO (p less than .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.
ARTICLES
The effect of nicardipine on neuronal function following ischemia
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