Strength, deformability, damage and fracture toughness of fibrous material networks: Application to fibrin clots.

A multiscale approach to mechanical testing in silico, which combines discrete particle-based simulations and large-deformation continuum mechanics, is developed to explore the mechanobiology, damage and fracture of fibrous materials. Combined with tensile testing in vitro of fibrin networks, the mechanical scaffold of blood clots, mechanisms of fibrin rupture are investigated that underlie embolization of intravascular blood clots (thrombi), a major cause of ischemic stroke and pulmonary embolism. At moderate strains (<50%), no network damage is observed. At larger strains, damage evolves and the network ruptures when only ∼5% of fibers and branch points break, opening a ∼150 µm rupture zone in silico. A continuum model that predicts macroscopic behavior for arbitrary states of deformation, including damage evolution, is constructed from the mesoscopic simulations with direct correlation of the damage parameter and the number of broken bonds in contrast to phenomenological damage laws. The continuum model can access length- and time-scales that are inaccessible in discrete simulations, which allows prediction of fracture toughness, the material property that determines rupture resistance in the presence of defects. This critical property for a fibrin network at physiological solid volume fraction and accounting for the dramatic decrease in volume (∼90%) under uniform tensile stressing is predicted to be 2.5-7.7 J/m, in good agreement with experiment. These insights into mechanisms of blood clot fracture can lead to the development of new approaches to predict and prevent embolization of intravascular thrombi. The multiscale approach developed is applicable to a wide range of fibrous network-based biomaterials. STATEMENT OF SIGNIFICANCE: Dummy.