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We study the dynamics of a compound liquid drop which is comprised of an outer membrane surface, a shell layer, and a core. The deformation due to an imposed extensional flow and the subsequent recovery are investigated computationally employing a combined Eulerian–Lagrangian technique. The numerical method allows for large viscosity and capillarity differences between layers. The present study reports several findings which provide direct insight into developing a dynamic model for leukocytes. A compound drop behaves like a homogeneous, simple liquid drop if the core is sufficiently deformed and the time scale of the core, related to the combination of its viscosity and capillarity, is comparable to that of the shell layer. Disparate time scales between the core and shell layer result in a rapid initial recoil of the drop during which the shell fluid is the primary participant in the hydrodynamics, followed by a slower relaxation period during which the core and shell layer interact with each other. Consequently, the apparent viscosity of the drop depends not only on the rheological properties of the drop, but also on the flow dynamics surrounding it. The findings obtained with the three-layer compound drop model can explain several main characteristics of leukocytes reported in the literature. Furthermore, our study suggests that unless the presence and possible deformation of the nucleus are explicitly accounted for, neither Newtonian nor non-Newtonian models for leukocytes can adequately predict the hydrodynamics of leukocytes.

Platelet activation, adhesion, and aggregation on the blood vessel and implants result in the formation of mural thrombi. Platelet dynamics in blood flow is influenced by the far more numerous erythrocytes (RBCs). This is particularly the case in the smaller blood vessels (arterioles) and in constricted regions of blood flow (such as in valve leakage and hinge regions) where the dimensions of formed elements of blood become comparable with that of the flow geometry. In such regions, models to predict platelet motion, activation, aggregation and adhesion must account for platelet-RBC interactions. This paper studies platelet-RBC interactions in shear flows by performing simulations of micro-scale dynamics using a computational fluid dynamics (CFD) model. A level-set sharp-interface immersed boundary method is employed in the computations in which RBC and platelet boundaries are tracked on a two-dimensional Cartesian grid. The RBCs are assumed to have an elliptical shape and to deform elastically under fluid forces while the platelets are assumed to behave as rigid particles of circular shape. Forces and torques between colliding blood cells are modeled using an extension of the soft-sphere model for elliptical particles. RBCs and platelets are transported under the forces and torques induced by fluid flow and cell-cell and cell-platelet collisions. The simulations show that platelet migration toward the wall is enhanced with increasing hematocrit, in agreement with past experimental observations. This margination is seen to occur due to hydrodynamic forces rather than collisional forces or volumetric exclusion effects. The effect of fluid shear forces on the platelets increases exponentially as a function of hematocrit for the range of parameters covered in this study. The micro-scale analysis can be potentially employed to obtain a deterministic relationship between fluid forces and platelet activation and aggregation in blood flow past cardiovascular implants.