Stroke, Vol 24, 1235-1240, Copyright © 1993 by American Heart Association
RL Zhang, M Chopp, H Chen, JH Garcia and ZG Zhang
BACKGROUND AND PURPOSE: We investigated the effect of hypothermia induced 1
hour after transient (2-hour) middle cerebral artery occlusion on the
extent of ischemic cell damage in the rat. METHODS: Middle cerebral artery
occlusion was induced extracranially by insertion of a nylon filament into
the right internal carotid artery. Two groups of rats were investigated:
(1) rats (n = 10) subjected to normothermic (37 degrees C) ischemia and
normothermic reperfusion; and (2) rats (n = 10) subjected to normothermic
ischemia and 1 hour of normothermic reperfusion followed by 3 hours of
hypothermia (30 degrees C). All rats were killed 1 week after the
experiment, and brain sections were stained with hematoxylin and eosin for
evaluation of ischemic cell damage. RESULTS: Infarct volume in normothermic
rats involved 20.9 +/- 4.6% of the hemisphere, whereas hypothermic rats
exhibited a significantly smaller (P < .001) infarct volume of 11.1 +/-
2.7%. The numbers of surviving (or structurally intact) neurons within
large sections of the cortex and striatum were significantly greater for
hypothermic compared with normothermic rats (P < .01). CONCLUSIONS: Our
data suggest that postischemic induction of hypothermia significantly
reduces ischemic cell damage after 2 hours of middle cerebral artery
occlusion in the rat, and that an interval of time of at least 1 hour after
ischemia exists in which hypothermic intervention is effective in either
salvaging or postponing irreversible neuronal injury.
ARTICLES
Postischemic (1 hour) hypothermia significantly reduces ischemic cell damage in rats subjected to 2 hours of middle cerebral artery occlusion
Department of Neurology, Henry Ford Hospital, Detroit, MI 48202.
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