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

Abstract

The influence of red blood cell (RBC) deformability in whole blood on platelet margination is investigated using confocal microscopy measurements of flowing human blood and cell resolved blood flow simulations. Fluorescent platelet concentrations at the wall of a glass chamber are measured using confocal microscopy with flowing human blood containing varying healthy-to-stiff RBC fractions. A decrease is observed in the fluorescent platelet signal at the wall due to the increase of stiffened RBCs in flow, suggesting a decrease of platelet margination due to an increased fraction of stiffened RBCs present in the flow. In order to resolve the influence of stiffened RBCs on platelet concentration at the channel wall, cellpair and bulk flow simulations are performed. For homogeneous collisions between RBC pairs, a decrease in final displacement after a collision with increasing membrane stiffness is observed. In heterogeneous collisions between healthy and stiff RBC pairs, it is found that the stiffened RBC is displaced most. The influence of RBC deformability on collisions between RBCs and platelets was found to be negligible due to their size and mass difference. For a straight vessel geometry with varying healthy-to-stiff RBC ratios, a decrease was observed in the red blood cell-free layer and platelet margination due to an increase in stiffened RBCs present in flow.

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.…”

Computational investigation of blood cell transport in retinal microaneurysms

“…Our results in Fig 7A (pink curve) show that the role of increased stiffness of RBCs in platelets transport in the MA channel is marginal. This finding is consistent with a prior study showing that the influence of RBC deformability on the collisions between RBCs and platelets was negligible [ 97 ]. We also compute the residence time of the platelets within MAs when the RBCs adhesion and increased RBC stiffness are considered.…”

Characterizing bulk rigidity of rigid red blood cell populations in sickle-cell disease patients

“…This damage to the endothelium led to inflammation, which causes endothelial dysfunction in SCD, contributing to crises 33 . Given that stiffened, HBS-rich RBCs have a higher propensity to marginate, i.e., migrate near the blood vessel wall 45 ,we anticipate these altered cells are likely well-positioned to cause endothelial damage regardless of their composition in blood. Thus, understanding the rigidity level of the HbS population can offer insight into crisis risk.…”