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(Stroke. 1995;26:1888-1892.)
© 1995 American Heart Association, Inc.

Articles

Reduction of Infarct Size by Intra-Arterial Nimodipine Administered at Reperfusion in a Rat Model of Partially Reversible Brain Focal Ischemia

José M. Roda, MD, PhD; Fernando Carceller, MD, PhD; Exuperio Díez-Tejedor, MD, PhD Carlos Avendaño, MD, PhD

From the Departments of Neurosurgery (J.M.R., F.C.), Neurology (E.D.-T.), and Experimental Surgery (J.M.R., F.C.), the Hospital "La Paz," and Department of Morphology (C.A.), Medical School, Autónoma University of Madrid, Spain.

Correspondence to Dr José M. Roda, c/Pedro Rico 13, 28029 Madrid, Spain.

Background and Purpose When blood flow to a brain region that has undergone an ischemic attack is reestablished, additional injury is to be expected from the reperfusion. The purpose of the study was to determine the effect of the intra-arterial injection of nimodipine at reperfusion on infarct volume in rats subjected to partially reversible focal neocortical ischemia.

Methods Two groups of Long-Evans rats with transient bilateral common carotid artery occlusion and permanent middle cerebral artery occlusion were subjected to retrograde cannulation of the external carotid artery close to the carotid bifurcation to allow the administration of isotonic saline (group 1) or nimodipine solution (group 2) just before and during reperfusion. The estimate for the actual amount of infarcted cortex was calculated by the volume ratio between the spared cortex in the infarcted hemisphere and the total cortex of the contralateral hemisphere by means of a stereological method based on the Cavalieri principle.

Results The percentage of cortex that was infarcted in control rats was 63.8±3.1%, whereas nimodipine-treated rats exhibited a significantly smaller (P<.005) percentage of infarct volume (31.3±12.7%).

Conclusions Our data show that the intra-arterial injection of nimodipine just before and during reperfusion reduced neocortical infarct volume in rats subjected to partially reversible focal cerebral ischemia.

Key Words: neuronal damage • neuroprotection • nimodipine • reperfusion • rats

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