EARLY MICROVASCULAR AND NEURONAL CONSEQUENCES OF TRAUMATIC BRAIN INJURY - A LIGHT AND ELECTRON-MICROSCOPIC STUDY IN RATS
EARLY MICROVASCULAR AND NEURONAL CONSEQUENCES OF TRAUMATIC BRAIN INJURY - A LIGHT AND ELECTRON-MICROSCOPIC STUDY IN RATS
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DOI：
10.1089/neu.1994.11.289
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发表时间：
1994-06-01
影响因子：
4.2
通讯作者：
HALLEY, M
中科院分区：
文献类型：
--
作者：
DIETRICH, WD;ALONSO, O;HALLEY, M
本研究的目的是记录麻醉的Sprague-Dawley大鼠中度创伤性脑损伤（TBI）的早期形态学结果。通过位于右大脑皮层上的靠近矢状面的损伤插管，用液压冲击脉冲（1.7-2.1 atm）损伤常温大鼠（37 ℃）（n = 7）。脑外伤后45 min，注射辣根过氧化物酶（HRP），15 min后灌注固定或浸泡固定，进行光镜和电镜观察。损伤半球的软脑膜表面和皮质浅层存在血脑屏障（BBB）对HRP的破坏。在外侧皮质的灰白色界面处也存在严重HRP渗漏的局灶性区域。该部位的光学显微镜检查显示与小静脉相关的瘀点。暗萎缩的神经元和肿胀的星形胶质细胞内检测皮质区覆盖的发展挫伤，CA 3和CA 4海马分区，和外侧丘脑。超微结构研究获得的证据不可逆的神经元损伤和机械损伤血管壁在这个早期创伤后时期。在非灌注创伤大鼠，管腔血小板聚集体也检测到出血部位。在这个模型中的TBI，微血管和神经元异常的一致模式可以记录在创伤后早期。这些早期变化的病理机制进行了讨论的原发性和继发性损伤过程。
The purpose of this study was to document the early morphologic consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats. Normothermic rats (37 degrees C) were injured with a fluid percussion pulse (1.7-2.1 atm) administered by an injury cannula positioned parasagittally over the right cerebral cortex (n = 7). At 45 min following TBI, rats were injected with the protein tracer horseradish peroxidase (HRP) and perfusion fixed or immersion fixed 15 min later for light and electron microscopic analysis. Blood-brain barrier (BBB) breakdown to HRP was present overlying the pial surface and superficial cortical layers of the injured hemisphere. A focal area of severe HRP leakage was also present at the gray-white interface of the lateral cortex. Light microscopic examination of this site revealed petechial hemorrhages associated with small venules. Dark shrunken neurons and swollen astrocytes were detected within cortical areas overlying the evolving contusion, CA3 and CA4 hippocampal subsectors, and lateral thalamus. Ultrastructural studies obtained evidence for irreversible neuronal injury and mechanical damage to vessel walls at this early posttraumatic period. In nonperfused traumatized rats, luminal platelet aggregates were also detected at sites of hemorrhage. In this model of TBI, a consistent pattern of microvascular and neuronal abnormalities can be documented in the early posttraumatic period. Pathomechanisms underlying these early changes are discussed in terms of primary and secondary injury processes.