Abstract
Vaso-occlusion, the stoppage of blood flow in sickle-cell disease, is a complex dynamical process spanning multiple time and length scales. Motivated by recent exvivo microfluidic measurements of hemostasis using blood from sickle-cell patients, we develop a multiphase model that couples the kinetics and hydrodynamics of a flowing suspension of normal and sickled cells in a fluid. We use the model to derive expressions for the cell velocities and concentrations that quantify the hydrodynamics of hemostasis, and provide simple criteria as well as a phase diagram for occlusion, consistent with our simulations and earlier observations.
Highlights
Motivated by recent ex vivo microfluidic measurements of hemostasis using blood from sickle-cell patients, we develop a multiphase model that couples the kinetics and hydrodynamics of a flowing suspension of normal and sickled cells in a fluid
We use the model to derive expressions for the cell velocities and concentrations that quantify the hydrodynamics of hemostasis, and provide simple criteria as well as a phase diagram for occlusion, consistent with our simulations and earlier observations
Hemoglobin A (HbA), the mutant protein, hemoglobin S (HbS), polymerizes to form filaments [2,3,4] under deoxygenated conditions typical of the venous system, a process that is reversible upon oxygenation in the lungs
Summary
Vaso-occlusion, the stoppage of blood flow in sickle-cell disease, is a complex dynamical process spanning multiple time and length scales. We consider the flow of blood, initially containing plasma and unsickled cells, through a capillary channel.
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