| Autor: |
Ramanujam RK; Department of Biomedical Engineering, Rutgers University, Piscataway, NJ, USA. vt280@soe.rutgers.edu., Garyfallogiannis K; Department of Mechanical Engineering and Applied Mechanics, University of Pennsylvania, Philadelphia, PA, USA., Litvinov RI; Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA, USA., Bassani JL; Department of Mechanical Engineering and Applied Mechanics, University of Pennsylvania, Philadelphia, PA, USA., Weisel JW; Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA, USA., Purohit PK; Department of Mechanical Engineering and Applied Mechanics, University of Pennsylvania, Philadelphia, PA, USA., Tutwiler V; Department of Biomedical Engineering, Rutgers University, Piscataway, NJ, USA. vt280@soe.rutgers.edu. |
| Abstrakt: |
Intravascular blood clots are subject to hydrodynamic shear and other forces that cause clot deformation and rupture (embolization). A portion of the ruptured clot can block blood flow in downstream vessels. The mechanical stability of blood clots is determined primarily by the 3D polymeric fibrin network that forms a gel. Previous studies have primarily focused on the rupture of blood plasma clots under tensile loading (Mode I), our current study investigates the rupture of fibrin induced by shear loading (Mode II), dominating under physiological conditions induced by blood flow. Using experimental and theoretical approaches, we show that fracture toughness, i.e. the critical energy release rate, is relatively independent of the type of loading and is therefore a fundamental property of the gel. Ultrastructural studies and finite element simulations demonstrate that cracks propagate perpendicular to the direction of maximum stretch at the crack tip. These observations indicate that locally, the mechanism of rupture is predominantly tensile. Knowledge gained from this study will aid in the development of methods for prediction/prevention of thrombotic embolization. |
