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Journal of Korean Neurosurgical Society 1996;25(1): 34-39.
Therapeutic Effect of Postischemic Selective Brain Cooling on Ischemic Brain Damage and Edema in focal Cerebral Infarction.
Choon Keun Park, Min Woo Baeik, Chong Min Park, Shin Soo Jun, Joon Ki Kang, Chang Rak Choi
1Department of Neurosurgery, Catholic University Medical College, Seoul, Korea.
2Department of Anesthesiology, Catholic University Medical College, Seoul, Korea.
ABSTRACT
The present study investigates the effect of temporary selective brain cooling(SBC) on ischemic brain damage and edema on permanent middle cerebral artery(MCA) occlusion in the rat. Eighteen adult male Sprague-Dawley rats weighing 300-400g were used under halothane anesthesia. The brain temperature was monitored in the left caudate nucleus through a burr hole in the middle of the left coronal suture. All animals underwent left MCA occlusion via subtemporal approach. During the surgery, the physiological variables including mean arterial blood pressure were monitored continuously. Three groups of animals were studied: group 1. Normothermic brain themperature control(n=6) ; group 2, brain cooling for 30min(n=6) ; and group 3, brain cooling for 60min(n=6). In all groups, rectal temperature was maintaind 36.5 degrees C~37 degrees C, and in groups 2 and 3, brain temperature was lowered to less than 34 degrees C by active cooling. 15 min following MCA occlusion. After the brain cooling treatment, anesthesia was discontinued, and the animals were returned to the cage. Twenty-four hours following MCA occlusion, the rats were sacrificed. The volume of ischemic damage and edema was obtained by frozen section technique. There were no significant differences in all physiological parameters between normothermic and hypothermic animals, except the brain temperature. Postischemic SBC for either 30 or 60min significantly reduced the volume of infarction in the cerebral hemisphrere by 14%(p<0.05) or by 27%(p<0.01) respectively and also attenuated neurologic deficits observed at 24 hour postocclusion. However the volume of ischemic brain edema was not significantly reduced and the ratio of volume of brain edema/infarction increased signficantly in groups 2(p<0.05) and 3(p<0.05) compared with group 1. The present study demonstrates that postischemic temporary BSC can attenuate hemispheric infarction in a permanent focal cerebral ichemia model in the rat. However, ischemic brain edema appears not to be attenuated at all. The mechanisms of hypothermic protection and its clinical application are discussed.
Key Words: Focal cerebral infarction; Hypothermia; Ischemic brain edema; Rats
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