Ahmadzadeh Hossein, Freedman Benjamin R, Connizzo Brianne K, Soslowsky Louis J, Shenoy Vivek B
Department of Materials Science and Engineering, University of Pennsylvania, Philadelphia, PA, USA.
McKay Orthopaedic Research Laboratory, University of Pennsylvania, Philadelphia, PA, USA.
Acta Biomater. 2015 Aug;22:83-91. doi: 10.1016/j.actbio.2015.04.035. Epub 2015 Apr 29.
As tendons are loaded, they reduce in volume and exude fluid to the surrounding medium. Experimental studies have shown that tendon stretching results in a Poisson's ratio greater than 0.5, with a maximum value at small strains followed by a nonlinear decay. Here we present a computational model that attributes this macroscopic observation to the microscopic mechanism of the load transfer between fibrils under stretch. We develop a finite element model based on the mechanical role of the interfibrillar-linking elements, such as thin fibrils that bridge the aligned fibrils or macromolecules such as glycosaminoglycans (GAGs) in the interfibrillar sliding and verify it with a theoretical shear-lag model. We showed the existence of a previously unappreciated structure-function mechanism whereby the Poisson's ratio in tendon is affected by the strain applied and interfibrillar-linker properties, and together these features predict tendon volume shrinkage under tensile loading. During loading, the interfibrillar-linkers pulled fibrils toward each other and squeezed the matrix, leading to the Poisson's ratio larger than 0.5 and fluid expulsion. In addition, the rotation of the interfibrillar-linkers with respect to the fibrils at large strains caused a reduction in the volume shrinkage and eventual nonlinear decay in Poisson's ratio at large strains. Our model also predicts a fluid flow that has a radial pattern toward the surrounding medium, with the larger fluid velocities in proportion to the interfibrillar sliding.
当肌腱受力时，它们的体积会减小，并向周围介质中渗出液体。实验研究表明，肌腱拉伸会导致泊松比大于0.5，在小应变时达到最大值，随后呈非线性衰减。在此，我们提出一种计算模型，将这种宏观观察结果归因于拉伸状态下原纤维之间载荷传递的微观机制。我们基于纤维间连接元件的力学作用开发了一个有限元模型，这些元件包括连接排列的原纤维的细纤维或纤维间滑动中的糖胺聚糖（GAGs）等大分子，并通过理论剪切滞后模型对其进行验证。我们揭示了一种以前未被认识到的结构 - 功能机制，即肌腱中的泊松比受施加的应变和纤维间连接物特性的影响，这些特征共同预测了拉伸载荷下肌腱体积的收缩。在加载过程中，纤维间连接物将原纤维相互拉近并挤压基质，导致泊松比大于0.5并排出液体。此外，在大应变下纤维间连接物相对于原纤维的旋转导致体积收缩减小，以及大应变下泊松比最终的非线性衰减。我们的模型还预测了一种向周围介质呈径向分布的流体流动，流体速度越大，与纤维间滑动成正比。
