Fracture resistance of blood clots plays a crucial role in physiological hemostasis and pathological thromboembolism. Although recent experimental and computational studies uncovered the poro-viscoelastic property of blood clots and its connection to the time-dependent deformation behavior, the effect of these physical processes on clot fracture and the underlying fracture mechanisms are not well understood. This work aims to formulate a thermodynamically consistent, multi-physics theoretical framework for describing the time-dependent deformation and fracture of blood clots. This theory concurrently couples fluid transport through porous fibrin networks, non-linear visco-hyperelastic deformation of the solid skeleton, solid–fluid interactions, mechanical degradation of tissues, gradient enhancement of energy, and protein unfolding of fibrin molecules. The constitutive relations of tissue constituents and the governing equation of fluid transport are derived within the framework of porous media theory by extending non-linear continuum thermodynamics at large strains. A physics-based, compressible network model is developed for the fibrin network of blood clots to describe its mechanical response. The kinetic equations of the internal variables, introduced for describing the non-linear viscoelastic deformation, non-local damage driving force and protein unfolding, are formulated according to the thermodynamics principles by incorporating a non-equilibrium energy of fibrin networks, a gradient-enhanced energy, and a stretch-induced energy of fibrin molecules, respectively, into the total free energy density function. An energy-based damage model is developed to predict the damage and fracture of blood clots, and an evolving regularization parameter is proposed to limit the damage zone bandwidth. The proposed model is implemented into finite element code by writing subroutines and is experimentally validated using single-edge cracked clot specimens with different constituents. The fracture of blood clots subject to different loading conditions is simulated, and the mechanisms of clot fracture are systematically analyzed. Computational results show that this model can accurately capture the experimentally measured deformation and fracture. The viscoelasticity and fluid transport play essential roles in the fracture of blood clots under physiological loading.

中文翻译：

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多孔粘超弹性诱导的血凝块时间依赖性骨折多物理场建模的理论框架


血凝块的抗断裂性在生理性止血和病理性血栓栓塞中起着至关重要的作用。尽管最近的实验和计算研究揭示了血凝块的多孔粘弹性特性及其与时间依赖性变形行为的联系，但这些物理过程对血凝块断裂的影响和潜在的骨折机制尚不清楚。这项工作旨在建立一个热力学一致的多物理场理论框架，用于描述血栓的时间依赖性变形和断裂。该理论同时耦合了通过多孔纤维蛋白网络的流体传输、固体骨架的非线性粘超弹性变形、固-液相互作用、组织的机械降解、能量的梯度增强和纤维蛋白分子的蛋白质去折叠。组织成分的本构关系和流体传递的控制方程是在多孔介质理论的框架内通过扩展大应变下的非线性连续热力学推导出来的。为血凝块的纤维蛋白网络开发了一种基于物理的可压缩网络模型，以描述其机械响应。根据热力学原理，通过将纤维蛋白网络的非平衡能、梯度增强能和纤维蛋白分子的拉伸诱导能分别纳入总自由能密度函数，建立了用于描述非线性粘弹性变形、非局部损伤驱动力和蛋白质去折叠的内部变量的动力学方程。 开发了一种基于能量的损伤模型来预测血栓的损伤和断裂，并提出了一个不断发展的正则化参数来限制损伤区带宽。所提出的模型通过编写子程序实现到有限元代码中，并使用具有不同成分的单边裂纹凝块样品进行了实验验证。模拟了不同负荷条件下血凝块的断裂，系统分析了凝块断裂的机制。计算结果表明，该模型能够准确捕捉实验测得的变形和断裂。粘弹性和流体输送在生理负荷下血栓的破裂中起着至关重要的作用。