Blast Overpressure in Rats: Recreating a Battlefield Injury in the Laboratory
Blast Overpressure in Rats: Recreating a Battlefield Injury in the Laboratory
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DOI：
10.1089/neu.2008.0748
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发表时间：
2009-06-01
影响因子：
4.2
通讯作者：
Bauman, Richard A.
中科院分区：
文献类型：
--
作者：
Long, Joseph B.;Bentley, Timothy L.;Bauman, Richard A.
脑爆炸伤是当前军事冲突中神经创伤的主要原因，其病因在很大程度上是不确定的。使用压缩驱动的激波管模拟爆炸效应，我们评估了空气爆炸暴露的生理、神经病理和神经行为后果，还评估了Kevlar防护背心对大鼠急性死亡率和幸存者创伤性脑损伤（TBI）发生率的影响。这种方法提供了可生存的爆炸条件下，TBI可以进行研究。126-和147-kPa的空气冲击波暴露引起了显著的神经病理学变化。凯夫拉背心，包裹胸部和腹部的一部分，大大降低了空气冲击波的死亡率，也改善了广泛的纤维变性，这是在暴露于126千帕的空气冲击波期间没有背心保护的大鼠大脑中突出的。这一发现指出了一个显着的贡献，其脑损伤的病理生理学的全身效应的空气冲击。这种强度的空气冲击波也会破坏神经和神经行为表现（e。例如，在一个实施例中，Morris水迷宫中的光束行走和空间导航采集）。随后立即发生出血性低血压，MAP维持在30 mm Hg，气流破坏心脏代偿性恢复，表现为峰值流出血量减少、达到峰值流出血量的时间和死亡时间。这些研究结果表明，休克管产生的气流可以导致TBI大鼠，部分通过全身调解，并由此产生的脑损伤显着影响急性心血管稳态机制以及神经行为功能。
Blast injury to the brain is the predominant cause of neurotrauma in current military conflicts, and its etiology is largely undefined. Using a compression-driven shock tube to simulate blast effects, we assessed the physiological, neuropathological, and neurobehavioral consequences of airblast exposure, and also evaluated the effect of a Kevlar (R) protective vest on acute mortality in rats and on the occurrence of traumatic brain injury (TBI) in those that survived. This approach provides survivable blast conditions under which TBI can be studied. Striking neuropathological changes were caused by both 126- and 147-kPa airblast exposures. The Kevlar vest, which encased the thorax and part of the abdomen, greatly reduced airblast mortality, and also ameliorated the widespread fiber degeneration that was prominent in brains of rats not protected by a vest during exposure to a 126-kPa airblast. This finding points to a significant contribution of the systemic effects of airblast to its brain injury pathophysiology. Airblast of this intensity also disrupted neurologic and neurobehavioral performance (e. g., beam walking and spatial navigation acquisition in the Morris water maze). When immediately followed by hemorrhagic hypotension, with MAP maintained at 30 mm Hg, airblast disrupted cardiocompensatory resilience, as reflected by reduced peak shed blood volume, time to peak shed blood volume, and time to death. These findings demonstrate that shock tube-generated airblast can cause TBI in rats, in part through systemic mediation, and that the resulting brain injury significantly impacts acute cardiovascular homeostatic mechanisms as well as neurobehavioral function.