Department of Biomedical Engineering, Wayne State University, 818 W. Hancock, Detroit, MI 48201, USA.
Ann Biomed Eng. 2012 Jan;40(1):227-36. doi: 10.1007/s10439-011-0420-4. Epub 2011 Oct 13.
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.
确定产生生理缺陷所需的超压对于推进暴露于爆炸中的个体的预防、诊断和治疗策略至关重要。在这项研究中，采用原发性爆炸神经创伤的啮齿动物模型来确定发生急性神经改变的压力。将大鼠暴露于 0、97、117 或 153 kPa 的单一低强度冲击波下。暴露后，使用 Morris 水迷宫评估大鼠的急性认知改变，使用水平梯测试评估大鼠的运动功能障碍。随后，对三个脑区（初级运动皮层、海马齿状回区域和后内侧皮质杏仁核）进行组织学分析。组织学参数包括测量胶质纤维酸性蛋白 (GFAP) 的水平以鉴定星形胶质细胞的激活、cleaved caspase-3 以鉴定早期细胞凋亡以及 Fluoro-Jade B (FJB)，其标记脑组织内的变性神经元。结果表明，与对照组和其他压力相比，暴露于单一 117 kPa 冲击波会导致整体神经缺陷发生显著变化。动物在水迷宫参数和 GFAP、caspase-3 和 FJB 阳性细胞数量上均出现明显改变。这表明，当暴露于低水平冲击波时，可能会在特定压力范围内引起生物力学反应，从而导致大鼠的低水平神经缺陷。这些数据表明，冲击波引起的神经创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明显和弥漫性的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，以阐明这种特定压力范围的现象。
