The effect of deformability on the microscale flow behavior of red blood cell suspensions

Abstract

Red blood cell (RBC) deformability is important for tissue perfusion and a key determinant of blood rheology. Diseases such as diabetes, sickle cell anemia, and malaria, as well as prolonged storage, may affect the mechanical properties of RBCs altering their hemodynamic behavior and leading to microvascular complications. However, the exact role of RBC deformability on microscale blood flow is not fully understood. In the present study, we extend our previous work on healthy RBC flows in bifurcating microchannels [Sherwood et al., "Viscosity and velocity distributions of aggregating and non-aggregating blood in a bifurcating microchannel," Biomech. Model. Mechanobiol. 13, 259-273 (2014); Sherwood et al., "Spatial distributions of red blood cells significantly alter local hemodynamics," PLoS One 9, e100473 (2014); and Kaliviotis et al., "Local viscosity distribution in bifurcating microfluidic blood flows," Phys. Fluids 30, 030706 (2018)] to quantify the effects of impaired RBC deformability on the velocity and hematocrit distributions in microscale blood flows. Suspensions of healthy and glutaraldehyde hardened RBCs perfused through straight microchannels at various hematocrits and flow rates were imaged, and velocity and hematocrit distributions were determined simultaneously using micro-Particle Image Velocimetry and light transmission methods, respectively. At low feed hematocrits, hardened RBCs were more dispersed compared to healthy ones, consistent with decreased migration of stiffer cells. At high hematocrit, the loss of deformability was found to decrease the bluntness of velocity profiles, implying a reduction in shear thinning behavior. The hematocrit bluntness also decreased with hardening of the cells, implying an inversion of the correlation between velocity and hematocrit bluntness with loss of deformability. The study illustrates the complex interplay of various mechanisms affecting confined RBC suspension flows and the impact of both deformability and feed hematocrit on the resulting microstructure.

Association between erythrocyte dynamics and vessel remodelling in developmental vascular networks

“…However, the magnitude of the changes in RBC deformability reported in the literature (ranging between 10% and 50% [38,65,66] to several folds [67,68]) would not support a model where such biomechanical changes alone are sufficient to cause vessel occlusion since previous studies showed that order of magnitude changes in shear modulus are required to impede RBC transit through narrow passages [46]. By contrast, our findings support a new concept where changes in the mechanical properties of the RBC membrane leading to abnormal haematocrit partitioning at bifurcations (via altered radial distributions of RBCs [69][70][71]) would reintroduce, in adult networks, the differences in WSS driving developmental vascular remodelling. Given the cross-species corroboration of important roles of WSS and RBC dynamics in vascular remodelling through different vertebrate model systems, future work should investigate the relevance of the findings to human physiology and whether the predicted WSS differences are sufficient to trigger pathological vascular remodelling.…”

Cross-sectional focusing of red blood cells in a constricted microfluidic channel

“…21 The effect of deformability on the microscale flow behavior of RBC suspensions has been studied previously. 25,30,42 Hur et al 21 used an gradually expanding microfluidic chip for classification of different types of cells based on their size and deformability. They showed that flexible cells occupy equilibrium positions much closer to the channel center compared to rigid cells and used this effect to conduct label-free cancer cell enrichment.…”

The influence of red blood cell deformability on hematocrit profiles and platelet margination

“…Recent microfluidic work reported that with an increase of stiffened RBCs present in flow, stiffened RBCs concentrate more toward the center-line of a 50μm wide channel [48], when compared to a healthy case. We do not observe a significant difference in stiff vs. healthy hematocrit profiles.…”