Histopathologic response of the immature rat to diffuse traumatic brain injury
Histopathologic response of the immature rat to diffuse traumatic brain injury
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DOI：
10.1089/08977150152693674
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发表时间：
2001-10-01
影响因子：
4.2
通讯作者：
Kochanek, PM
中科院分区：
文献类型：
--
作者：
Adelson, PD;Jenkins, LW;Kochanek, PM
本研究的目的是描述大鼠在出生后第17天（PND）发生撞击加速度弥漫性创伤性脑损伤（TBI）后的组织病理学反应，该损伤采用150-g/2-m损伤，如前所述。这种损伤产生急性神经和生理紊乱以及持久的运动和Morris水迷宫（MWM）功能缺陷。分别于伤后1、3、7、28、90 d对灌注固定的脑组织进行大体检查和HE染色、Bielschowsky银染色、胶质细胞酸性蛋白（GFAP）免疫组化光镜观察。大体病理检查显示1-3天时弥漫性蛛网膜下腔出血（SAH），但幕上脑实质内出血轻微。在腹侧脑干节段和小脑中观察到点状出血。存活1-3天后，光学显微镜显示弥漫性SAH和脑室内出血（IVH），轻度水肿，明显的轴突损伤，反应性星形胶质细胞增生和局部中线小脑出血。轴突损伤最常发生在脑干的长的上行和下行纤维束，偶尔在前脑，并在3天最大，但直到7天后受伤。反应性星形胶质细胞在位置和时间上都类似，但在海马、白色物质束和胼胝体中也明显发现。通常，TBI产生显著的弥漫性SAH，伴有脑和脑干星形胶质细胞增生和轴突损伤，但无明显的神经元丢失。由于这种损伤产生了类似于婴儿和儿童TBI的持续性功能障碍的病理变化，因此对于进一步研究弥漫性TBI和未成熟脑中脑干损伤的病理生理和治疗是有用的。
The purpose of this study was to characterize the histopathologic response of rats at postnatal day (PND) 17 following an impact-acceleration diffuse traumatic brain injury (TBI) using a 150-g/2-meter injury as previously described. This injury produces acute neurologic and physiologic derangements as well as enduring motor and Morris water maze (MWM) functional deficits. Histopathologic studies of perfusion-fixed brains were performed by gross examination and light microscopy using hematoxylin and eosin, Bielschowsky silver stain, and glial fibrillary acidic protein (GFAP) immunohistochemistry at 1, 3, 7, 28, and 90 day after injury. Gross pathologic examination revealed diffuse subarachnoid hemorrhage (SAH) at 1-3 days but minimal supratentorial intraparenchymal hemorrhage. Petechial hemorrhages were noted in ventral brainstem segments and in the cerebellum. After 1-3-day survivals, light microscopy revealed diffuse SAH and intraventricular hemorrhage (IVH), mild edema, significant axonal injury, reactive astrogliosis, and localized midline cerebellar hemorrhage. Axonal injury most commonly occurred in the long ascending and descending fiber tracts of the brainstem and occasionally in the forebrain, and was maximal at 3 days, but present until 7 days after injury. Reactive astrocytes were similarly found both in location and timing, but were also significantly identified in the hippocampus, white matter tracts, and corpus callosum. Typically, TBI produced significant diffuse SAH accompanied by cerebral and brainstem astrogliosis and axonal injury without obvious neuronal loss. Since this injury produces some pathologic changes with sustained functional deficits similar to TBI in infants and children, it should be useful for the further study of the pathophysiology and therapy of diffuse TBI and brainstem injury in the immature brain.