Postischemic (1 hour) hypothermia significantly reduces ischemic cell damage in rats subjected to 2 hours of middle cerebral artery occlusion.

Abstract

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.

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@article{Zhang1993PostischemicH, title={Postischemic (1 hour) hypothermia significantly reduces ischemic cell damage in rats subjected to 2 hours of middle cerebral artery occlusion.}, author={Rui Zhang and Michael Chopp and Huan Chen and Julio H. Garcia and Z Gang Zhang}, journal={Stroke}, year={1993}, volume={24 8}, pages={1235-40} }