| Abstract: |
| The size, formation time, and structure of a blood clot depends on the local hemodynamics, transmural pressure, and the nature and size of the injury where the clot is forming. Here we studied extravascular clotting, where blood leaks from a main vessel into the extravascular space. The goal was to better understand how transmural pressures across an injury and injury size affect clot structure and occlusion times. Our approach was using a mathematical model of platelet aggregation and coagulation. The model is based on a continuum approach to track the advection, diffusion, and aggregation of platelet densities in a dynamic fluid environment. We also developed a simplified model of coagulation that considers generation of coagulation enzymes at the injury walls and on the platelet surfaces. We used a finite volume method in a T-shaped geometry where blood flows through a main top channel and escapes through a downward injury channel. We found that higher pressures led to very dense homogenous clots and low pressures led to less dense heterogenous clots. Some clots that occluded in larger injuries continued to grow into the main channel where this was not seen with smaller injuries. |
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