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Acta Neurochir. Suppl. · Jan 1998
Effects of mild and moderate hypothermia on cerebral metabolism and glutamate in an experimental head injury.
- K Mori, M Maeda, M Miyazaki, and H Iwase.
- Department of Neurosurgery, Juntendo University, Izunagaoka Hospital, Japan.
- Acta Neurochir. Suppl. 1998 Jan 1;71:222-4.
AbstractIn this study we sought to determine the optimal brain temperature for treating compression-induced cerebral ischemia. Six cats each were treated with a deep-brain temperature of 37 degrees C (control), 33 degrees C (mild hypothermia), or 29 degrees C (moderate hypothermia). Intracranial pressure (ICP) and cerebral blood flow (CBF) were monitored, as were arteriovenous oxygen difference (AVDO2) and cerebral venous oxygen saturation (ScvO2). The cerebral metabolic rate of oxygen (CMRO2) was calculated. Extracellular glutamate concentration was measured by microdialysis. ICP was increased by inflation of an epidural balloon until CBF became zero. This ischemia was maintained for 5 min, after which the balloon was deflated. Mild hypothermia showed coupled CBF-metabolic suppression, but moderate hypothermia resulted in disproportionately increased AVDO2, decreased ScvO2, and low CBF/CMRO2 (relative ischemia). Reactive hyperemia after balloon deflation was decreased after both mild and moderate hypothermia, as was the tissue volume showing Evans blue dye extravasation. Extracellular glutamate increased in control animals, an effect most effectively suppressed in the mild hypothermia group. These data favor 33 degrees C as the optimal temperature for treating compression-related cerebral ischemia.
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