Cerebral Artery Occlusion

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°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°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. (Stroke 1993;24:1235-1240)