This title appears in the Scientific Report : 2015 
Microvascular blood flow resistance: Role of red blood cell migration and dispersion
Katanov, Dinar (Corresponding Author)
Gompper, Gerhard / Fedosov, Dmitry (Corresponding Author)
Theorie der Weichen Materie und Biophysik; IAS-2
Theorie der Weichen Materie und Biophysik; ICS-2
Microvascular research, 99 (2015) S. 57-66
Orlando, Fla. Academic Press 2015
10.1016/j.mvr.2015.02.006
Journal Article
Physical Basis of Diseases
Please use the identifier: http://dx.doi.org/10.1016/j.mvr.2015.02.006 in citations.


Microvascular blood flow resistance has a strong impact on cardiovascular function and tissue perfusion. The flow resistance in microcirculation is governed by flow behavior of blood through a complex network of vessels, where the distribution of red blood cells across vessel cross-sections may be significantly distorted at vessel bifurcations and junctions. In this paper, the development of blood flow and its resistance starting from a dispersed configuration of red blood cells is investigated in simulations for different hematocrit levels, flow rates, vessel diameters, and aggregation interactions between red blood cells. Initially dispersed red blood cells migrate toward the vessel center leading to the formation of a cell-free layer near the wall and to a decrease of the flow resistance. The development of cell-free layer appears to be nearly universal when scaled with a characteristic shear rate of the flow. The universality allows an estimation of the length of a vessel required for full flow development, lc ≲ 25D, for vessel diameters in the range 10 μm < D < 100 μm. Thus, the potential effect of red blood cell dispersion at vessel bifurcations and junctions on the flow resistance may be significant in vessels which are shorter or comparable to the length lc. Aggregation interactions between red blood cells generally lead to a reduction of blood flow resistance. The simulations are performed using the same viscosity for both external and internal fluids and the RBC membrane viscosity is not considered; however, we discuss how the viscosity contrast may affect the results. Finally, we develop a simple theoretical model which is able to describe the converged cell-free-layer thickness at steady-state flow with respect to flow rate. The model is based on the balance between a lift force on red blood cells due to cell-wall hydrodynamic interactions and shear-induced effective pressure due to cell–cell interactions in flow. We expect that these results can also be used to better understand the flow behavior of other suspensions of deformable particles such as vesicles, capsules, and cells.