Miyazawa T, Hossmann K A
Department of Nerurosurgery, National Defense Medical College, Saitama, Japan.
No To Shinkei. 1994 Jan;46(1):29-37.
The effect of manipulating the brain temperature during cerebral ischemia was investigated in Wistar rats subjected to 30 min 4-vessel occlusion. Three brain temperature profiles were compared: 1. Spontaneous decrease in brain temperature during ischemia from 36 to 31 degrees C (spontaneous hypothermia; n = 5); 2. Constant brain temperature of 30 degrees C induced by selective head cooling (induced hypothermia; n = 5); and 3. Constant brain temperature of 36 degrees C induced by selective heating of the head (normothermia; n = 5). The core temperature was maintained constant at 37 degrees C in all groups. In the spontaneously hypothermic brains, 16% of the CA1 neurons survived after 30 min ischemia. Induced hypothermia significantly increased this percentage to 69%, but maintenance of the brain temperature at normothermia decreased neuronal survival to 1%. Normothermia of the brain also led to morphological injury outside the vulnerable regions, greater variability of the morphologic lesions, an increase in mortality, a marked loss of body weight, and prolongation of EEG suppression, as compared to in both hypothermic groups. These findings clearly demonstrate that maintaining the brain temperature at normothermia by selective heating of the head aggravates ischemic injury and, in consequence, should not be used to investigate the effectiveness of protective drugs for brain ischemia.
在接受30分钟四血管闭塞的Wistar大鼠中，研究了脑缺血期间调控脑温的效果。比较了三种脑温模式：1. 缺血期间脑温从36℃自发下降至31℃（自发低温；n = 5）；2. 通过选择性头部降温诱导的30℃恒定脑温（诱导低温；n = 5）；3. 通过选择性头部加热诱导的36℃恒定脑温（正常体温；n = 5）。所有组的核心体温均维持在37℃恒定。在自发低温的脑中，缺血30分钟后16%的CA1神经元存活。诱导低温显著将该百分比提高至69%，但将脑温维持在正常体温会使神经元存活率降至1%。与两个低温组相比，脑的正常体温还导致易损区域外的形态学损伤、形态学损伤的更大变异性、死亡率增加、体重显著减轻以及脑电图抑制时间延长。这些发现清楚地表明，通过选择性头部加热将脑温维持在正常体温会加重缺血损伤，因此，不应将其用于研究脑缺血保护药物的有效性。
