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首页> 外文期刊>Journal of Biomechanics >Temporal development of hippocampal cell death is dependent on tissue strain but not strain rate
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Temporal development of hippocampal cell death is dependent on tissue strain but not strain rate

机译：海马细胞死亡的时间发展取决于组织应变而不是应变率

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Deformation of brain tissue in response to mechanical loading of the head is the root-cause of traumatic brain injury (TBI). Even below ultimate failure limits, deformation activates pathophysiological cascades resulting in delayed cell death. Injury response of soft tissues, such as the chest and spinal cord, is dependent on the product of deformation and velocity, a parameter termed the viscous criterion. We set out to test if hippocampal cell death could be predicted by a similar combination of strain and strain rate and if the viscous criterion was valid for hippocampus. Quantitative prediction of the brain's biological response to mechanical stimuli is difficult to achieve in animal models of TBI, so we utilized an in vitro model of TBI based on hippocampal slice cultures. We quantified the temporal development of cell death after precisely controlled deformations for 30 combinations of strain (0.05-0.50) and strain rate (0.1-50 s(-1)) relevant to TBI. Loading conditions for a subset of cultures were verified by analysis of highspeed video. Cell death was found to be significantly dependent on time-post injury, on strain magnitude, and to a lesser extent, on anatomical region by a repeated-measures, three-way ANOVA. The responses of the CA1 and CA3 regions of the hippocampus were not statistically different in contrast to some in vivo TBI studies. Surprisingly, cell death was not dependent on strain rate leading us to conclude that the viscous criterion is not a valid predictor for hippocampal tissue injury. Given the large data set and extensive combinations of biomechanical parameters, predictive mathematical functions relating independent variables (strain, region, and time post-injury) to the resultant cell death were defined. These functions can be used as tolerance criteria to equip finite element models of TBI with the added capability to predict biological consequences. (c) 2005 Elsevier Ltd. All rights reserved.
机译：头部机械负荷引起的脑组织变形是创伤性脑损伤（TBI）的根本原因。即使低于极限极限，变形也会激活病理生理级联反应，导致细胞死亡延迟。软组织（如胸部和脊髓）的损伤反应取决于变形和速度的乘积，该乘积被称为粘性标准。我们着手测试是否可以通过应变和应变率的类似组合预测海马细胞死亡，以及粘性标准对海马是否有效。在TBI的动物模型中很难对大脑对机械刺激的生物学反应进行定量预测，因此我们基于海马切片培养物使用了TBI的体外模型。我们对与TBI相关的30种应变（0.05-0.50）和应变率（0.1-50 s（-1））组合进行精确控制的变形后，量化了细胞死亡的时间发展。通过分析高速视频验证了部分文化的加载条件。通过重复测量三向方差分析，发现细胞死亡与创伤后时间，应变大小以及解剖区域有显着相关性。与某些体内TBI研究相比，海马CA1和CA3区的反应没有统计学差异。出人意料的是，细胞死亡并不取决于应变率，这使我们得出结论，粘性标准不是海马组织损伤的有效预测因子。给定大量数据集和生物力学参数的广泛组合，定义了将独立变量（损伤后的应变，区域和时间）与导致的细胞死亡相关的预测数学函数。这些功能可以用作公差标准，为TBI的有限元模型配备预测生物学后果的附加功能。 （c）2005 Elsevier Ltd.保留所有权利。

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