% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Katanov:190082,
author = {Katanov, Dinar and Gompper, Gerhard and Fedosov, Dmitry},
title = {{M}icrovascular blood flow resistance: {R}ole of red blood
cell migration and dispersion},
journal = {Microvascular research},
volume = {99},
issn = {0026-2862},
address = {Orlando, Fla.},
publisher = {Academic Press},
reportid = {FZJ-2015-03041},
pages = {57-66},
year = {2015},
abstract = {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.},
cin = {IAS-2 / ICS-2},
ddc = {610},
cid = {I:(DE-Juel1)IAS-2-20090406 / I:(DE-Juel1)ICS-2-20110106},
pnm = {553 - Physical Basis of Diseases (POF3-553)},
pid = {G:(DE-HGF)POF3-553},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000354420200007},
doi = {10.1016/j.mvr.2015.02.006},
url = {https://juser.fz-juelich.de/record/190082},
}