Stroke, Vol 23, 273-279, Copyright © 1992 by American Heart Association
AM Buchan, D Xue and A Slivka
BACKGROUND AND PURPOSE: We describe a new rat model of temporary focal
ischemia that produces neocortical ischemia without the need for prolonged
anesthesia. METHODS: Temporary focal cerebral ischemia was initiated during
halothane anesthesia, maintained for varying periods without anesthesia,
and reversed by clip removal requiring brief anesthesia. Tandem carotid and
middle cerebral artery occlusion for 1-4 hours and permanent occlusion were
used to determine the duration and extent of ischemia necessary to produce
predictable volumes of neocortical infarction in Wistar and spontaneously
hypertensive rats. RESULTS: In Wistar rats, occlusion of the right middle
cerebral and both common carotid arteries resulted in cerebral blood flow
reductions to approximately 8% of baseline. One hour of transient ischemia
with 23 hours of reperfusion did not result in infarction. Three hours of
ischemia followed by 21 hours of reperfusion resulted in infarction
comparable to that caused by 24 hours of permanent ischemia. In
spontaneously hypertensive rats, unilateral right middle cerebral and
common carotid artery occlusion reduced cerebral blood flow to
approximately 11% of baseline. Minimal damage was seen with 1 hour of
reversible ischemia, but intervals of 2 and subsequently 3 hours followed
by 22-21 hours of reperfusion produced progressively larger infarcts.
Damage indistinguishable from that seen with 24 hours of permanent ischemia
was seen with 3 or 4 hours of transient ischemia followed by 21 or 20 hours
of reperfusion. CONCLUSIONS: For unanesthetized normothermic rats, cerebral
blood flow reductions to 10- 20% of baseline resulted in maximal infarction
once ischemic durations exceeded 2-3 hours. To be effective, experimental
therapies aimed at lessening infarct size or restoring blood flow must be
initiated within this critical time interval.
ARTICLES
A new model of temporary focal neocortical ischemia in the rat
Laboratory of Cerebral Ischemia, Robarts Research Institute, London.
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