Stroke, Vol 20, 268-274, Copyright © 1989 by American Heart Association
J Kucharczyk, W Chew, N Derugin, M Moseley, C Rollin, I Berry and D Norman
We investigated whether the calcium channel entry blocker nicardipine would
reduce ischemic brain damage in barbiturate-anesthetized cats subjected to
permanent unilateral occlusion of the middle cerebral artery. The evolution
of cerebral injury was assessed in vivo in 24 cats by a combination of
proton magnetic resonance imaging and phosphorus-31 magnetic resonance
spectroscopy for 5 hours following occlusion. Immediately thereafter, the
volume of histochemically ischemic brain tissue was determined
planimetrically in triphenyl tetrazolium chloride-stained serial coronal
sections. Nicardipine was initially administered as an intravenous bolus
injection of 10 mg/kg/hr 15 minutes before or 15 minutes after occlusion,
followed by continuous infusion at 8 mg/kg/hr for the 5 hours of the
experiment. Compared with untreated controls, cats that received
nicardipine before or after occlusion showed a significant reduction in the
extent of edema in the ipsilateral cerebral cortex, internal capsule, and
basal ganglia. The results of phosphorus-31 magnetic resonance spectroscopy
studies suggest that nicardipine may protect against cerebral ischemic
damage by an action on cellular metabolic processes that preserve
high-energy phosphates during the ischemic period.
ARTICLES
Nicardipine reduces ischemic brain injury. Magnetic resonance imaging/spectroscopy study in cats
Department of Radiology, School of Medicine, University of California, San Francisco 94143.
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