Breakdown of the blood-brain barrier after fluid percussion brain injury in the rat: Part 2: Effect of hypoxia on permeability to plasma proteins.
Breakdown of the blood-brain barrier after fluid percussion brain injury in the rat: Part 2: Effect of hypoxia on permeability to plasma proteins.
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大鼠液体冲击脑损伤后血脑屏障的破坏：第 2 部分：缺氧对血浆蛋白通透性的影响。
DOI：
10.1089/neu.1992.9.335
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发表时间：
1992
影响因子：
4.2
通讯作者：
Noble,LJ
中科院分区：
文献类型：
--
作者：
Tanno,H;Nockels,RP;Pitts,LH;Noble,LJ
临床研究表明，严重脑损伤后缺氧是常见的，并显著影响神经功能。因此，我们建立了一个大鼠创伤后缺氧损伤模型，以确定脑损伤后的病理生理反应，这种二次损伤恶化。我们研究了脑损伤后缺氧对血脑屏障对血浆蛋白渗透性的影响。动物分为两个实验组：I组（单独冲击）和IH组（冲击加缺氧）。使大鼠经受侧向流体膨胀性脑损伤（4.8- 5.2atm）。IH组动物伤后立即暴露于10%O2的低氧环境中45 min。在每组中，在光学显微镜水平检查血管对内源性免疫球蛋白（IgG）和辣根过氧化物酶（HRP）的通透性。IgG在损伤后1-24 h在脑切片中免疫定位。在其他研究中，HRP在撞击前或杀死前10分钟静脉注射。在损伤后1-72小时评估对该蛋白的渗透性。伤后1h各组渗出蛋白的分布相似。明显异常的渗透性IgG和HRP（前的影响）发生在离散区域的同侧和对侧半球。损伤后6小时，注意到组I和IH之间的血脑屏障的差异反应。在IH组的损伤半球中观察到广泛的蛋白质渗漏。这一发现与第一组形成鲜明对比，在第一组中，外渗的蛋白质更多地位于受伤的半球。测定HRP重建血脑屏障的时间进程（在处死前给予）。冲击部位保持渗透到至少72小时内组I和IH伤后HRP。I组伤后6 h，脑皮质深部和脑皮质旁血脑屏障重建。IH组伤后24 h血脑屏障才恢复。这些研究表明：（1）脑损伤后缺氧加剧了血脑屏障对循环蛋白的局部破坏，（2）缺氧对通透性的影响在损伤后立即不明显，而是在损伤后6小时表达，（3）创伤性脑损伤后缺氧延迟了血脑屏障的恢复。这些结果表明，继发性创伤后缺氧有助于脑损伤的血管发病机制。
Clinical studies have demonstrated that hypoxia after severe brain injury is common and significantly worsens neurologic outcome. We have, therefore, developed a rat model of posttraumatic hypoxic injury in order to identify the pathophysiologic responses after head injury that are worsened by this secondary insult. We examined the effect of hypoxia after brain injury on permeability of the blood–brain barrier to plasma proteins. Animals were divided into two experimental groups: group I (impact alone) and group IH (impact plus hypoxia). Rats were subjected to a lateral fluid percussive brain injury (4.8–5.2 atm). Animals in group IH were exposed to hypoxic conditions (10% O2) for 45 min immediately after injury. In each group, vascular permeability to endogenous immunoglobulins (IgG) and to horseradish peroxidase (HRP) was examined at the light microscopic level. IgG was immunolocalized in brain sections at 1–24 h after injury. In other studies, HRP was given i.v. either before impact or 10 min before killing. Permeability to this protein was assessed at 1–72 h after injury. The distribution of extravasated proteins was similar between the experimental groups at 1 h postinjury. Pronounced abnormal permeability to IgG and HRP (given before impact) occurred in discrete regions throughout both the ipsilateral and contralateral hemispheres. By 6 h after injury, a differential response of the blood–brain barrier was noted between groups I and IH. Widespread leakage of proteins was observed in the injured hemisphere in group IH. This finding was in sharp contrast to group I, in which extravasated proteins remained more localized in the injured hemisphere. The time course for reestablishment of the blood–brain barrier to HRP (given before killing) was determined. The impact site remained permeable to HRP up to at least 72 h postinjury within groups I and IH. In group I, the blood–brain barrier was reestablished in the parasagittal cortex and deep cortical layer by 6 h postinjury. In contrast, the blood–brain barrier in group IH was not restored in similar brain regions until 24 h postinjury. These studies demonstrate that (1) hypoxia after brain injury exacerbates the regional breakdown of the blood–brain barrier to circulating proteins, (2) this influence of hypoxia on permeability is not apparent immediately after injury but rather is expressed at 6 h after injury, and (3) hypoxia after traumatic brain injury delays recovery of the blood–brain barrier. These findings suggest that secondary posttraumatic hypoxia contributes to the vascular pathogenesis of brain injury.
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影响因子：
6.3
作者：
ISHIGE, N;PITTS, LH;WEINSTEIN, PR
通讯作者：
WEINSTEIN, PR
头部损伤和脑缺血——对治疗的影响。
影响因子：
9.8
作者：
J. Miller
通讯作者：
J. Miller
缺氧对大鼠脑外伤的影响：第1部分：神经功能、脑电图和组织病理学的变化。
影响因子：
4.8
作者：
N. Ishige;L. Pitts;T. Hashimoto;M. Nishimura;H. Bartkowski
通讯作者：
H. Bartkowski
缺氧对大鼠脑外伤的影响：第二部分：高能磷酸盐代谢的变化。
影响因子：
4.8
作者：
N. Ishige;L. Pitts;L. Pogliani;T. Hashimoto;M. Nishimura;H. Bartkowski;T. James
通讯作者：
T. James
影响因子：
6.3
作者：
DOBBIN, J;CROCKARD, HA;ROSSRUSSELL, R
通讯作者：
ROSSRUSSELL, R