Stroke, Vol 22, 1032-1039, Copyright © 1991 by American Heart Association
B Kaplan, S Brint, J Tanabe, M Jacewicz, XJ Wang and W Pulsinelli
We investigated the temporal threshold for focal cerebral infarction in the
spontaneously hypertensive rat. The right middle cerebral artery and common
carotid artery were occluded for 0, 1, 2, 3, 4, or 24 hours, and all the
animals were sacrificed 24 hours after the onset of ischemia. Cortical
infarct volumes and edema volumes were quantified in serial frozen sections
of hematoxylin and eosin-stained tissue using image analysis. Upon
occlusion, blood flow in the core of the ischemic zone, measured with
laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7%
of the preocclusion baseline value (n = 26). During the first hour of
ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of
baseline (n = 25). Release of the middle cerebral artery and common carotid
artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of
baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no
infarction, while ischemic intervals of 2 and 3 hours produced successively
larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours'
duration followed by approximately 20 hours of recirculation yielded
infarct volumes that were not significantly different from those after 24
hours of permanent focal ischemia. The results indicate that 3-4 hours of
focal cerebral ischemia in this rat model is sufficient to attain maximal
infarction and suggest that recirculation or pharmacological interventions
after this time will provide little benefit.
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Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia
Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021.
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