Chronic histopathological consequences of fluid-percussion brain injury in rats: Effects of post-traumatic hypothermia
Chronic histopathological consequences of fluid-percussion brain injury in rats: Effects of post-traumatic hypothermia
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DOI：
10.1007/s004010050602
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发表时间：
1997-02-01
影响因子：
12.7
通讯作者：
Busto, R
中科院分区：
文献类型：
--
作者：
Bramlett, HM;Dietrich, WD;Busto, R
实验性创伤性脑损伤（TBI）的早期结果测量对于表征创伤的严重程度以及阐明神经元脆弱性模式的病理机制是有用的。然而，越来越明显的是，急性结局指标可能并不总是慢性结局的准确预测因子，特别是在评估潜在治疗方案的疗效时。本研究检查了慢性组织病理学结果，在大鼠8周后，液体水肿TBI加上中度创伤后脑低温，一个协议，提供急性神经元保护。动物接受中度副脑水肿性头部损伤（2.01-2.38 atm）或假手术，随后立即进行3小时的脑低温（30 ℃）或常温（37 ℃）。TBI后8周，连续组织切片用苏木精和伊红染色或对胶质细胞酸性蛋白进行免疫染色。在同侧丘脑、海马和损伤部位外侧的新皮质中观察到组织损伤、神经胶质增生和免疫反应性星形胶质细胞。在丘脑内，局灶性坏死仅限于选择性丘脑核团。两组脑外伤患者的同侧齿状回门区海马细胞明显丢失。定量体积测量结果显示，在两个TBI组的影响同侧的皮质，丘脑和海马体积显着减少。TBI正常体温组的侧脑室大幅扩大，TBI后低温显着减弱了这种效应。通过创伤后低温的侧脑室扩张的衰减指示该TBI模型中的慢性神经保护。这些数据提供了新的信息有关的慢性组织病理学后果的实验TBI和相关性的创伤模型，慢性人类头部损伤。
Early outcome measures of experimental traumatic brain injury (TBI) are useful for characterizing the traumatic severity as well as for clarifying the pathomechanisms underlying patterns of neuronal vulnerability. However, it is increasingly apparent that acute outcome measures may not always be accurate predictors of chronic outcome, particularly when assessing the efficacy of potential therapeutic regimens. This study examined the chronic histopathological outcome in rats 8 weeks following fluid-percussive TBI coupled with moderate posttraumatic brain hypothermia, a protocol that provides acute neuronal protection. Animals received a moderate parasagittal percussive head injury (2.01-2.38 atm) or sham procedure followed immediately by 3 h of brain hypothermia (30 degrees C) or normothermia (37 degrees C). Eight weeks following TBI, serial tissue sections were stained with hematoxylin and eosin or immunostained for glial fibrillary acidic protein. Tissue damage, gliosis and immunoreactive astrocytes were observed in the ipsilateral thalamus, hippocampus, and in the neocortex lateral to the injury site. Within the thalamus, focal necrosis was restricted to selective thalamic nuclei. Significant hippocampal cell loss was found in the ipsilateral dentate hilar region of both TBI groups. Quantitative volume measurements revealed significant decreases in cortical, thalamic and hippocampal volume ipsilateral to the impact in both TBI groups. Lateral ventricles were substantially enlarged in the TBI-normothermia group, an effect which was significantly attenuated by post-TBI hypothermia. The attenuation of lateral ventricular dilation by post-traumatic hypothermia is indicative of chronic neuroprotection in this TBI model. These data provide new information concerning the chronic histopathological consequence of experimental TBI and the relevance of this trauma model to chronic human head injury.