Bramlett H M, Dietrich W D, Green E J, Busto R
Neurotrauma Research Center, University of Miami, Florida 33101, USA.
Acta Neuropathol. 1997 Feb;93(2):190-9. doi: 10.1007/s004010050602.
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 post-traumatic 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.
实验性创伤性脑损伤（TBI）的早期结果测量对于表征创伤严重程度以及阐明神经元易损性模式背后的病理机制很有用。然而，越来越明显的是，急性结果测量可能并不总是慢性结果的准确预测指标，尤其是在评估潜在治疗方案的疗效时。本研究检查了在流体冲击性TBI并伴有中度创伤后脑低温（一种提供急性神经元保护的方案）8周后的大鼠慢性组织病理学结果。动物接受中度矢状旁冲击性头部损伤（2.01 - 2.38大气压）或假手术，随后立即进行3小时的脑低温（30摄氏度）或正常体温（37摄氏度）。TBI后8周，连续组织切片用苏木精和伊红染色或进行胶质纤维酸性蛋白免疫染色。在同侧丘脑、海马以及损伤部位外侧的新皮质中观察到组织损伤、胶质增生和免疫反应性星形胶质细胞。在丘脑中，局灶性坏死局限于选择性丘脑核。在两个TBI组的同侧齿状门区均发现明显的海马细胞丢失。定量体积测量显示，两个TBI组中冲击同侧的皮质、丘脑和海马体积均显著减小。TBI - 正常体温组的侧脑室明显扩大，TBI后脑低温可显著减轻这种效应。创伤后脑低温对侧脑室扩张的减轻表明该TBI模型具有慢性神经保护作用。这些数据提供了关于实验性TBI慢性组织病理学后果以及该创伤模型与慢性人类头部损伤相关性的新信息。
