Platelet margination dynamics in blood flow: The role of lift forces and red blood cells aggregation

Homeostasis plays a critical role in maintaining the delicate balance between preventing excessive bleeding and enabling clot formation during injuries. One pivotal aspect of homeostasis involves the development of platelet clots. In this study, we analyze numerically the behavior of platelet margination as a function of the adhesion energy between red blood cells (RBCs), driven by the presence of plasma proteins. We examine scenarios encompassing both physiological conditions and pathological states, such as those seen in patients with diabetes. Employing a two-dimensional simulation, we utilize rigid particles and a vesicle model to simulate platelets and RBCs, respectively. We employ the lattice Boltzmann method to solve the underlying model equations. We first demonstrate that platelet margination is primarily determined by lift forces and is not notably affected by whether the cells undergo tank-treading (TT) or tumbling (TB) behavior, as often reported. Specifically, we unveil instances where cells exhibit TT or TB behavior, yet their platelet concentration profiles closely resemble each other. Furthermore, we present a striking result concerning the impact of RBC adhesion. In microcirculation the hematocrit is in the range $5–20\%$. A moderate adhesion energy (falling within the physiological range) boosts platelet margination in microcirculation. However, this effect becomes small for larger hematocrit encountered in macrocirculation (e.g., $40\%$). This boost is more significant for a viscosity contrast (viscosity of cytoplasm over that the suspending fluid) equal to a known value for RBCs, as compared to the case without viscosity contrast. As we increase the adhesion energy (the pathological range), a noteworthy decline in platelet margination is found, albeit that for some flow strength the platelet margination reaches a minimum and increases again at higher adhesion energy. These results can be attributed to a combination of lift generated by the bounding walls and the formation of RBC clusters. Notably, our study sheds light on a critical consequence of excessive adhesion, typically observed in pathological conditions like diabetes mellitus.