Mori K, Maeda M, Miyazaki M, Iwase H
Department of Neurosurgery, Juntendo University, Izunagaoka Hospital, Shizuoka, Japan.
Neurol Res. 1998 Dec;20(8):719-26. doi: 10.1080/01616412.1998.11740590.
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.
研究了轻度（33摄氏度）和中度（29摄氏度）低温的效果，以确定哪个温度对压迫性脑缺血更有效。18只猫被麻醉。根据脑深部温度将动物分为三组（对照组，37摄氏度；轻度低温组，33摄氏度；中度低温组，29摄氏度）。监测颅内压（ICP）和脑血流量（CBF），后者通过氢清除率来监测。在上矢状窦采集的血样中测量动静脉氧差（AVDO2）和脑静脉血氧饱和度（ScvO2）。计算脑氧代谢率（CMRO2）和脑乳酸代谢率（CMR乳酸）。通过微透析测量细胞外谷氨酸。通过向硬膜外气囊充气使ICP升高，直到CBF变为零，这种缺血状态维持5分钟，之后迅速放气。所有参数在6小时内记录。注射伊文思蓝以检查血管通透性变化。轻度低温使CBF降低56%，中度低温使其降低77%。轻度低温伴有代谢抑制，而中度低温显著增加AVDO2并降低ScvO2，导致低CBF/CMRO2（相对缺血）。气囊放气后，所有三组均出现反应性充血，轻度和中度低温使其显著减轻。然后CBF降至充气前值的50%，ScvO2降低（缺血后灌注不足）。三组之间CBF/CMRO2、ScvO2和AVDO2无显著差异。气囊放气后，所有三组的CMR乳酸均升高，轻度和中度低温使其显著降低。对照组动物的细胞外谷氨酸增加（3.8±1.72微摩尔），轻度低温组（1.0±0.46微摩尔）对这种效应的抑制最为有效。伊文思蓝染料外渗所示的损伤组织体积在对照组为729±89立方毫米，轻度低温组为247±56立方毫米，中度低温组为267±35立方毫米。这些数据表明，轻度低温（33摄氏度）可能是治疗压迫性脑缺血的最佳脑温。
