MARKED PROTECTION BY MODERATE HYPOTHERMIA AFTER EXPERIMENTAL TRAUMATIC BRAIN INJURY
MARKED PROTECTION BY MODERATE HYPOTHERMIA AFTER EXPERIMENTAL TRAUMATIC BRAIN INJURY
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DOI：
10.1038/jcbfm.1991.13
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发表时间：
1991-01-01
影响因子：
6.3
通讯作者：
HAYES, RL
中科院分区：
文献类型：
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作者：
CLIFTON, GL;JIANG, JY;HAYES, RL
这些实验检测了亚低温对大鼠实验性创伤性脑损伤(TBI)后死亡率和神经功能障碍的影响。所有实验均采用脑实质内探头连续测量脑温。全麻下(1.5%氟烷/70%一氧化二氮/30%氧气)在水浴(0℃)中局部浸泡(皮肤用塑料屏障保护)诱导脑降温。在实验I中，我们研究了损伤前诱导的亚低温对液压冲击伤后死亡率的影响。伤前将大鼠降温至36℃(n=16)、33℃(n=17)、30℃(n=11)，伤后维持在目标温度1h。大脑温度降低30摄氏度，死亡率显著降低(p<；0.04)。36摄氏度、33摄氏度和30摄氏度的死亡率分别为37.5%、41%和9.1%。在实验II中，我们考察了颅脑损伤后启动的亚低温或高温对长期行为缺陷的影响。大鼠于伤后5min开始降温至36℃(n=10)、33℃(n=10)或30℃(n=10)，或升温至38℃(n=10)或40℃(n=12)，并在目标温度下维持1h。与常温(38℃)大鼠相比，亚低温治疗大鼠的横梁行走、横梁平衡和体重减轻明显减少。在30摄氏度的低温组观察到最大的保护作用。由于体表降温可以在人体内诱导30摄氏度的温度，而不会出现凝血障碍或室颤，因此30摄氏度的低温在治疗人脑损伤方面可能具有潜在的临床价值。
These experiments examined the effects of moderate hypothermia on mortality and neurological deficits observed after experimental traumatic brain injury (TBI) in the rat. Brain temperature was measured continuously in all experiments by intraparenchymal probes. Brain cooling was induced by partial immersion (skin protected by a plastic barrier) in a water bath (0-degrees-C) under general anesthesia (1.5% halothane/70% nitrous oxide/30% oxygen). In experiment I, we examined the effects of moderate hypothermia induced prior to injury on mortality following fluid percussion TBI. Rats were cooled to 36-degrees-C (n = 16), 33-degrees-C (n = 17), or 30-degrees-C (n = 11) prior to injury and maintained at their target temperature for 1 h after injury. There was a significant (p < 0.04) reduction in mortality by a brain temperature of 30-degrees-C. The mortality rate at 36-degrees-C was 37.5%, at 33-degrees-C was 41%, and at 30-degrees-C was 9.1%. In experiment II, we examined the effects of moderate hypothermia or hyperthermia initiated after TBI on long-term behavioral deficits. Rats were cooled to 36-degree-C (n = 10), 33-degrees-C (n = 10), or 30-degrees-C (n = 10) or warmed to 38-degrees-C (n = 10) or 40-degrees-C (n = 12) starting at 5 min after injury and maintained at their target temperatures for 1 h. Hypothermia-treated rats had significantly less beam-walking, beam-balance, and body weight loss deficits compared to normothermic (38-degrees-C) rats. The greatest protection was observed in the 30-degrees-C hypothermia group. Since a temperature of 30-degrees-C can be induced in humans by surface cooling without coagulopathy or ventricular fibrillation, hypothermia to 30-degrees-C may have potential clinical value for treatment of human brain injury.