Effects of mild (33 degrees C) and moderate (29 degrees C) hypothermia on cerebral blood flow and metabolism, lactate, and extracellular glutamate in experimental head injury.
The effects of mild (33 degrees C) and moderate (29 degrees C) hypothermia were investigated to determine which temperature was more effective against compression-induced cerebral ischemia. Eighteen cats were anesthetized. The animals were divided into three groups according to deep-brain temperature (control, 37 degrees C; mild hypothermia, 33 degrees C; and moderate hypothermia, 29 degrees C). Intracranial pressure (ICP) and cerebral blood flow (CBF) were monitored, the latter by hydrogen clearance. Arteriovenous oxygen difference (AVDO2) and cerebral venous oxygen saturation (ScvO2) were measured in blood samples from the superior sagittal sinus. The cerebral metabolic rate of oxygen (CMRO2) and the cerebral metabolic rate of lactate (CMR lactate) were calculated. Extracellular glutamate was measured by microdialysis. ICP was increased by inflation of an epidural balloon until CBF became zero, and this ischemia was maintained for 5 min, after which the balloon was quickly deflated. All parameters were recorded over 6 h. Evans blue was injected to examine vascular permeability changes. CBF was decreased by 56% by mild hypothermia and by 77% by moderate hypothermia. Mild hypothermia had a coupled metabolic suppression whereas moderate hypothermia significantly increased AVDO2 and decreased ScvO2, producing a low CBF/CMRO2 (relative ischemia). After balloon deflation, all three groups showed reactive hyperemia, which was significantly reduced by mild and moderate hypothermia. CBF then decreased to 50% of pre-inflation values and ScvO2 decreased (post-ischemic hypoperfusion). CBF/CMRO2, ScvO2, and AVDO2 did not differ significantly between the three groups. After balloon deflation, all three groups showed increased CMR lactate, which was significantly reduced by mild and moderate hypothermia. Extracellular glutamate increased in control animals (3.8 +/- 1.72 microM), an effect most effectively suppressed in the mild hypothermia group (1.0 +/- 0.46 microM). Damaged tissue volumes as indicated by Evans blue dye extravasation were 729 +/- 89 mm3 in control, 247 +/- 56 mm3 in mild hypothermia, and 267 +/- 35 mm3 in moderate hypothermia animals. These data suggest that mild hypothermia (33 degrees C) might be the optimal brain temperature to treat compression-related cerebral ischemia.
Mori
K
K
Department of Neurosurgery, Juntendo University, Izunagaoka Hospital, Shizuoka, Japan.
Maeda
M
M
Miyazaki
M
M
Iwase
H
H
D000818:Animals; D001831:Body Temperature; D001921:Brain / Q000098:blood supply / Q000378:metabolism; D001923:Brain Chemistry / Q000502:physiology; D002245:Carbon Dioxide / Q000032:analysis; D002404:Catheterization; D002415:Cats; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006259:Craniocerebral Trauma / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D004195:Disease Models, Animal; D005070:Evans Blue / Q000493:pharmacokinetics; D018698:Glutamic Acid / Q000378:metabolism*; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D007773:Lactates / Q000378:metabolism*; D010100:Oxygen / Q000032:analysis; D010101:Oxygen Consumption / Q000502:physiology
D007773:Lactates; D002245:Carbon Dioxide; D018698:Glutamic Acid; D005070:Evans Blue; D010100:Oxygen