Mori K, Maeda M, Miyazaki M, Iwase H
Department of Neurosurgery, Juntendo University, Izunagaoka Hospital, Japan.
Acta Neurochir Suppl. 1998;71:222-4. doi: 10.1007/978-3-7091-6475-4_64.
In 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.
在本研究中,我们试图确定治疗压迫性脑缺血的最佳脑温。每组6只猫分别接受37℃(对照组)、33℃(轻度低温)或29℃(中度低温)的脑深部温度治疗。监测颅内压(ICP)和脑血流量(CBF),以及动静脉氧差(AVDO2)和脑静脉血氧饱和度(ScvO2)。计算脑氧代谢率(CMRO2)。通过微透析测量细胞外谷氨酸浓度。通过向硬膜外气囊充气使ICP升高,直至CBF变为零。这种缺血状态维持5分钟,之后气囊放气。轻度低温显示CBF与代谢呈耦合性抑制,但中度低温导致AVDO2不成比例增加、ScvO2降低以及CBF/CMRO2较低(相对缺血)。轻度和中度低温后,气囊放气后的反应性充血均降低,出现伊文思蓝染料外渗的组织体积也减小。对照组动物的细胞外谷氨酸增加,这种效应在轻度低温组中得到最有效的抑制。这些数据表明33℃是治疗压迫相关脑缺血的最佳温度。