Mild Neurotrauma Indicates a Range-Specific Pressure Response to Low Level Shock Wave Exposure
Mild Neurotrauma Indicates a Range-Specific Pressure Response to Low Level Shock Wave Exposure
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DOI：
10.1007/s10439-011-0420-4
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发表时间：
2012-01-01
影响因子：
3.8
通讯作者：
Bir, Cynthia A.
中科院分区：
文献类型：
--
作者：
VandeVord, Pamela J.;Bolander, Richard;Bir, Cynthia A.
确定造成生理缺陷所需的超压水平对于推进爆炸暴露个体的预防、诊断和治疗策略至关重要。在这项研究中，采用啮齿动物原发性爆炸神经损伤模型来确定发生急性神经改变的压力。在0、97、117和153 kPa的压力下，将大鼠暴露在单一低强度冲击波中。暴露后，用Morris水迷宫评估大鼠的急性认知改变，用水平阶梯测试评估运动功能障碍。随后，对三个脑区（初级运动皮层、海马齿状回区和后内侧皮质杏仁核）进行组织学分析。组织学参数包括测定胶质纤维酸性蛋白（GFAP）水平以识别星形胶质细胞活化，测定cleaved caspase-3水平以识别早期凋亡，测定脑组织内标记变性神经元的Fluoro-Jade B （FJB）水平。结果表明，与对照组和其他压力相比，暴露于单个117千帕冲击波显示出总体神经功能缺损的显着变化。动物的水迷宫参数发生了显著变化，GFAP、caspase-3和fjb阳性细胞的数量在组织学上增加。这表明，当暴露于低水平的冲击波时，可能存在由特定压力范围引起的生物力学反应，从而导致大鼠的低水平神经功能障碍。这些数据表明，冲击波引起的神经损伤可能导致大鼠短期学习和记忆的认知缺陷。额外的组织学证据支持显著和弥漫性胶质细胞激活和细胞损伤。需要进一步研究冲击波暴露的生物力学方面，以阐明这种压力范围特定的现象。
Identifying the level of overpressure required to create physiological deficits is vital to advance prevention, diagnostic, and treatment strategies for individuals exposed to blasts. In this study, a rodent model of primary blast neurotrauma was employed to determine the pressure at which acute neurological alterations occurred. Rats were exposed to a single low intensity shock wave at a pressure of 0, 97, 117, or 153 kPa. Following exposure, rats were assessed for acute cognitive alterations using the Morris water maze and motor dysfunction using the horizontal ladder test. Subsequently, histological analyses of three brain regions ( primary motor cortex, the hippocampal dentate gyrus region, and the posteromedial cortical amygdala) were conducted. Histological parameters included measuring the levels of glial fibrillary acidic protein (GFAP) to identify astrocyte activation, cleaved caspase-3 for early apoptosis identification and Fluoro-Jade B (FJB) which labels degenerating neurons within the brain tissue. The results demonstrated that an exposure to a single 117 kPa shock wave revealed a significant change in overall neurological deficits when compared to controls and the other pressures. The animals showed significant alterations in water maze parameters and a histological increase in the number of GFAP, caspase-3, and FJB-positive cells. It is suggested that when exposed to a low level shock wave, there may be a biomechanical response elicited by a specific pressure range which can cause low level neurological deficits within the rat. These data indicate that neurotrauma induced from a shock wave may lead to cognitive deficits in short-term learning and memory of rats. Additional histological evidence supports significant and diffuse glial activation and cellular damage. Further investigation into the biomechanical aspects of shock wave exposure is required to elucidate this pressure range-specific phenomenon.