Haslach Henry W, Leahy Lauren N, Hsieh Adam H
Department of Mechanical Engineering, University of Maryland, College Park, MD 20742, USA.
Department of Mechanical Engineering, University of Maryland, College Park, MD 20742, USA.
J Mech Behav Biomed Mater. 2015 Aug;48:12-27. doi: 10.1016/j.jmbbm.2015.04.003. Epub 2015 Apr 8.
An external mechanical insult to the brain may create internal deformation waves, which have shear and longitudinal components that induce combined shear and compression of the brain tissue. To isolate such interactions and to investigate the role of the extracellular fluid (ECF) in the transient mechanical response, translational shear stretch up to 1.25 under either 0 or 33% fixed normal compression is applied without preconditioning to heterogeneous sagittal slices which are nearly the full length of the rat brain cerebrum. The normal stress contribution is estimated by separate unconfined compression stress-stretch curves at 0.0667/s and 1/s engineering strain rates to 33% strain. Unconfined compression deformation causes lateral dimension expansion less than that predicted for an incompressible material under large deformation and often a visible loss of internal fluid from the specimen so that the bulk brain tissue is not incompressible in vitro, as sometimes assumed for mathematical modeling. The response to both slow 0.001/s and moderate 1/s shear translational stretch rates is deformation rate dependent and hardening under no compression but under 33% compression is nearly linear perhaps because of increased solid-solid friction. Both shear and normal stress relaxation are faster after the fast rate deformation possibly because higher deformation rates produce higher ECF hydrostatic pressure that primarily drives stress relaxation. The experimental results on ECF behavior guide the form of our nonlinear viscoelastic mathematical model. Our data are closely fit by non-equilibrium evolution equations that involve at most three specimen-specific empirical parameters and that are based on the idea that stretch of axons and glial processes resists load-induced ECF pressure.
对大脑的外部机械损伤可能会产生内部变形波，这种波具有剪切和纵向分量，会导致脑组织受到剪切和压缩的联合作用。为了分离这种相互作用并研究细胞外液（ECF）在瞬态机械响应中的作用，在0或33%的固定法向压缩下，对几乎是大鼠大脑半球全长的异质矢状切片施加高达1.25的平移剪切拉伸，且不进行预处理。通过在0.0667/s和1/s的工程应变率下对33%应变的单独无侧限压缩应力-拉伸曲线来估计法向应力贡献。无侧限压缩变形导致横向尺寸膨胀小于大变形下不可压缩材料预测的膨胀，并且通常会有明显的内部液体从标本中流失，因此体外的大块脑组织并非如数学建模有时假设的那样不可压缩。对0.001/s的慢速和1/s的中速剪切平移拉伸速率的响应都与变形速率有关，在无压缩时会硬化，但在33%压缩下几乎呈线性，这可能是由于固-固摩擦力增加所致。快速变形后，剪切应力和法向应力松弛都更快，这可能是因为较高的变形速率会产生更高的ECF静水压力，而这种压力主要驱动应力松弛。关于ECF行为的实验结果指导了我们非线性粘弹性数学模型的形式。我们的数据与非平衡演化方程紧密拟合，这些方程最多涉及三个特定于标本的经验参数，并且基于轴突和神经胶质过程的拉伸抵抗负载诱导的ECF压力这一观点。
