Posttraumatic hypothermia in the treatment of axonal damage in an animal model of traumatic axonal injury
Posttraumatic hypothermia in the treatment of axonal damage in an animal model of traumatic axonal injury
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DOI：
10.3171/jns.1998.89.2.0303
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发表时间：
1998-08-01
影响因子：
4.1
通讯作者：
Povlishock, JT
中科院分区：
文献类型：
--
作者：
Koizumi, H;Povlishock, JT
物体。许多研究人员已经证明了低温对动物和人类创伤性脑损伤(TBI)的保护作用。典型的，：他的保护已经被评估与神经元的保存和/或行为异常的钝化有关。然而，对于颅脑损伤所致轴突损伤这一人类脑损伤的特征，几乎没有考虑到任何潜在的保护作用。在本研究中，作者评价了低温对大鼠TBT后轴突损伤的保护作用。雄性SD大鼠体重380~400g，采用冲击加速装置进行实验性颅脑损伤。这些大鼠在损伤前或损伤后接受低温处理，将其颞肌和直肠温度维持在32摄氏度，持续1小时。在这个1小时的低温期后，在90分钟内复温到常温水平。24小时后，动物被处死，并对大脑的半矢状面进行反应，以显示淀粉样前体蛋白(APP)，这是轴突损伤的标志。计算每只动物脑桥延髓连接处皮质脊髓束内APP标记的受损轴突的密度。在所有体温过低的动物中，APP明显损伤的轴突密度显著降低。在损伤前、损伤后即刻和延迟低温治疗的动物中，损伤轴突的密度与未治疗的对照组相比显著降低(p<；0.05)。作者根据这些发现推断，早期和延迟的创伤后低温对脑外伤有实质性的保护作用，至少在损伤的轴突方面是这样。
Object. Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals and humans. Typically,:his protection has been evaluated in relation to the preservation of neurons and/or the blunting of behavioral abnormalities. However, little consideration has been given to any potential protection afforded in regard to TBI-induced axonal injury, a feature of human TBI. In this study, the authors evaluated the protective effects of hypothermia on axonal injury after TBT in rats.Methods. Male Sprague-Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subjected to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32 degrees C for 1 hour. After this I-hour period of hypothermia, rewarming to normothermic levels was accomplished over a 90-minute period. Twenty-four hours later, the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the amyloid precursor protein (APP), a marker of axonal injury. The density of APP-marked damaged axons within the corticospinal tract at the pontomedullary junction was calculated for each animal. In all hypothermic animals, a significant reduction in APP-marked damaged axonal density was found. In animals treated with preinjury, immediate postinjury, and delayed hypothermia, the density of damaged axons was dramatically reduced in comparison with the untreated controls (p < 0.05).Conclusions. The authors infer from these findings that early as well as delayed posttraumatic hypothermia results in substantial protection in TBI, at least in terms of the injured axons.