You are on page 1of 73

ABSTRACT

Key words: two-phase hemodynamics model, multiphase disperse systems,


cell depleted layer, blood flow modelling, Fahraeus effect, Fahraeus-Lindqvist
effect.
At present time cardiovascular diseases take place as a leading cause of
deaths in developed countries. Development of vascular surgery and functional
diagnostics methods led to growth of a quality of treatment. To estimate a
lesion degree the different invasive methods are used. But at the last time a
non-invasive diagnostics method are used too. For example, there are many
mathematical models of cardiovascular system. But the main part of them
don’t take to attention the rheological properties of blood. These features
are appeared because blood consists of suspension of plasma and blood cells.
The main part of last ones are erythrocytes. In result the cell depleted layer
appears in microvessels. More over a viscosity depends not only hematocrit but
it depends on vessel size too.
A suspension of plasma and blood cells can be described in context of
theory of multiphase disperse system.
Despite the rheological properties of blood generally appears in microves-
sels, the construction of multiphase models for big vessels is actual task. Be-
cause in case of stenotic vessels there is a narrowing part of the ones. In case
of hemodynamic significant stenosis some part of vessel have a little radius. So
in this case the rheological properties of blood can appear. Taken into account
all above said we receive the following.
The purpose of this study is to develop a model of non-stationary two-
phase hemodynamics in stenosis based on the rheology of the non-Newtonian
liquid.
The object of the study is a blood flow in coronary arteries in case of
stenotic wall.
The subject of the study is theoretical investigation and numerical simu-
lation of coronary arteries hemodynamics with using the rheological properties
of blood.
In the first chapter we describe the results of recent investigations in blood
flow hemodynamics.
In the second chapter the main known results of functional bases of coro-
nary blood flow are presented. In this chapter we describe base moments of
disperse system theory.
In the third chapter we present a base equations of the multiphase system
theory. This chapter consists the axially symmetric collisionless equations of
two-phase systems too which we transform from Cartesian coordinate.
At the forth chapter the main results are presented. It is an axially sym-
metrical collisionless model of two-phase hemodynamics. Further an axially
symmetrical mixture model is done too. The numerical simulation results are
done in cases of normal and stenotic vessels. The main results which are pre-
sented in this chapter consist in the following.
ˆ An axially-symmetric collisionless model of two-phase hemodynamics is
done.
ˆ An axially-symmetric mixture model of two-phase blood flow and a single
phase hemodynamics model is presented.
ˆ Axially-symmetric mixture model is adapted to numerical simulation of
blood flow in stenotic vessels in Comsol Multiphysics.
It was received that
ˆ a volume fraction of the RBCs depends on radius and a geometry of vessel
and small depends on the initial and boundary distribution,
ˆ a cell depleted layer appear near the vessel wall and near a stenosis,
ˆ there is a high hematocrit zone in region behind stenosis.
At the end we present a comparative analysis of the numerical simulations.
The study is ended by conclusion.
The results of this investigation was reported at the scientific seminars of
General and Experimental Physics Department of TSU.
CONTENTS

List of abbreviations 4

Introduction 5

1 Computational models of blood flow 7


1.1 Single-phase blood flow modelling 7
1.2 Two-phase hemodynamics 9

2 Physiological bases of coronary blood flow 12


2.1 Rheology of blood 12
2.1.1 Basic principles of the theory of disperse system 12
2.1.2 Blood as a disperse media 13
2.2 Functional features of coronary arteries 15

3 Basics of the multiphase disperse media theory 19


3.1 Equations of the multiphase hydrodynamics 19
3.2 Equations of the two-phase hydrodynamics in cylindrical coordinates 23
3.3 Mixture model equations 26

4 Two-phase vascular blood flow models 29


4.1 Two-phase axially symmetrical collisionless model of hemodynamics 29
4.1.1 The first case of hematocrit function 32
4.1.2 The second case of hematocrit function 35
4.2 Single-phase laminar blood flow 37
4.3 Two-phase mixture model 40
4.3.1 Numerical simulation in case of normal vessels 42
4.3.2 Numerical simulation in case of stenotic vessels 48
4.4 Comparative analysis of the numerical simulations 52
Conclusion 60

References 62

3
LIST OF ABBREVIATIONS

LCA Left coronaty artery


LMCA Main stem of the left coronary artery
LAD Left anterior descending artery
Cx Circumflex artery
RCA Right coronary artery
PDA Posterior descending artery
FFR Fraction flow reserve
RBC Red blood cell
RBCs Red blood cells
MRI Magnetic resonance imaging

4
INTRODUCTION

Development of computer technologies has led to successful application


of numerical simulation in different branches of medicine. Herewith computer
models of blood flow enable to receive different hemodynamics parameters by
noninvasive methods. The modern surgical techniques and methods of func-
tional diagnostics define the success in treatment of cardiovascular diseases [17].
It must be marked that narrowing of blood vessel diameter is one of the reasons
of hemodynamics injury . As result the oxygen supply of tissues is decreased
and the ischemia appears.
An information about the incidence of stenosis influences on the choice of
treatment tactic. The combination of different diagnostics is used to receive
data about vessel state.The coronary angiography often well demonstrates the
percent of vessel decreasing at stenotic region. Herewith if there is a diffusion,
concentric and symmetric injury then this stenosis will be visualized as a nor-
mal vessel [17]. Therefor the coronary angiography is supplemented by other
methods. For example, the intravascular ultrasound allows to receive informa-
tion about atheromatous plaques also in diffusion injury. In the last time the
method of fractional flow reserve (FFR) is appeared. It allows to determine
the hemodynamic significance of the stenosis but it is an invasive procedure.
In this case the numerical simulations can be used for FFR calculation in some
stenosis or group of stenosis.
Herewith if we consider a group of stenosis then we can not receive infor-
mation about which stenosis is more hemodynamic significance by using the
coronary angiography, the intravascular ultrasound or FFR of blood flow. This
information have the significance to choose the stenosis for surgery treatment.
In some cases it may be choose only one stenotic part of vessel for coronary stent
and hemodynamics may be recovered. In this situation noninvasive computer
modelling can be used too.

5
There are many different methods of numerical simulation in hemody-
namics. They are based on the finite element analysis. In the last time the
models of two-phase hemodynamics are used for investigation of microcircu-
lation [2, 14, 30, 31]. Most often the continuous phase corresponds to plasma
and discret phase is determinated by characteristics of the red blood cells. In
microvessels the rheological features of the blood are becoming significance,
namely: correlation between vessel size and blood viscosity, Fahraeus and
Fahraeus-Lindqvist effects and existence of the cell-free layer [10, 20, 55]. Nev-
ertheless, the single-phase flow models of viscous incompressible liquid are well
adapted for numerical simulation of blood flow in big vessels. In case of steno-
sis the narrowing parts of vessel appear and non-Newtonian rheological features
of blood may be hemodynamic significance. In these conditions, the using of
two-phase hemodynamics is of interest to the study.
Taken into account all above mentioned the construction of the two-phase
non-stationary hemodynamics model is relevant for the study of the coronary
artery stenosis influence to blood flow.
The purpose of this study is to develop a model of non-stationary two-
phase hemodynamics in stenosis based on the rheology of the non-Newtonian
liquid. During the work, the following tasks are solved:
ˆ receiving of two-phase hemodynamic equations in cylindricaly-symmetric
coordinate system,
ˆ construction of an axially symmetrical collisionless model of two-phase
hemodynamics in Comsol Multiphysics,
ˆ construction of axially symmetrical models of single-phase and two-phase
mixture flows in case of stenosis and without it in Comsol Multiphysics,
ˆ comparison of numerical calculations results for different models.

6
1 Computational models of blood flow

The results of many researchers of XVI – XIX centuries lie in the base of
modern hemodynamics. For example, the Hagen–Poiseuille law [56,61] gives the
velocity in case of laminar stationary liquid flow through cylinder. As known it
has the parabolic profile. Herewith Yong and Weber [23] studied a wave motion
in elastic tubes. In result Moens and Korteweg received the known formula
s
Eh
v= .
2ρR

It set the dependence of the wave velocity v from such parameters as the Young
modulus E, a thickness of tube wall h, a radius of tube R and density of tube
wall ρ.
It was be mentioned that the motion equations of hemodynamics are
Navier–Stokes equations. Herewith the modern scientific results admit to di-
vided all hemodynamic models to single-phase and multiphase models. In first
the single-phase models appeared.

1.1 Single-phase blood flow modelling

The one of the first blood flow model is, so named, Frank model. It is based
on the conceptions of Windkessel theory [11]. Frank suggested that artery is an
elastic tube, herewith pulse flow runs in the vessel and stationary flow runs out
the vessel. In the systole phase blood flows in a vessel and in the diastole phase
it flows out. The Frank model uses the finite velocity of wave propagation.
Opposite to Frank suggestions Hamilton assumed that pressure wave have
infinite velocity in an aorta but in peripheral vessels it is finite too [23].
In [62] Womersley solved the linearized Navier–Stokes equation for a rigid
vessel. It was considered that a vessel is an infinite cylinder for which a wall’s
thickness is more smaller then its radius. Further [63] elastic features of vessels
were taken into consideration. In the next researches a pulse wave reflection [64]

7
and a variable viscosity [65] were taken into account too. There are many models
which are based on the Womersley model. The description of such models is
presented in [7].
One of many classes of hemodynamics models is a set of analogous or
lumped-parameter models [22,23,27,51]. These models are based on the analogy
between blood and electric current flow. In this case a heart corresponds to
power element with alternating electromotive force and vascular network is
replaced by set of resistances and capacitances. Herewith voltage relates to
pressure and current relates to blood flow. Then these characteristics satisfy
an equation similar to the Ohm’s law. As known hemodynamic parameters of
blood flow do not calculate well enough for lumped-parameter models [8]. So
it is a disadvantage of the corresponding simulations.
The next big class of hemodynamics models connects with hydrodynamic
equations considered in 1d, 2d or 3d modelling. One dimensional models ad-
mit to calculate blood flow parameters for all vascular network which is rep-
resented by one dimensional graph. These models are described by average
Navier–Stokes equation [23, 34, 42]. Two and three dimensional hemodynam-
ics models admit to simulate a curved and branched network of vessels more
exactly. They are described by Navier–Stokes equation and require more com-
puting resources. These models is often used for numerical investigation of
different vascular anomaly or curved and bifurcated vessels [4, 48]. It must be
marked the study [6] which defines a correlation between bifurcation angle at
the left coronary artery and hemodynamics.
In the last time there are numerical simulations which are used different
approaches in one model. It may be either combination of lumped-parameter
model and 2d or 3d modelling either combination of 1d-model and 2d or 3d
simulation. In these cases lumped-parameter models or 1d simulations are used
for calculating of boundary conditions for 2d or 3d modeling which are described
a blood flow in a fixed vessel. For example, in [43] a lumped parameter coronary

8
vascular bed model calculates inlet and outlet conditions for three-dimensional
vessel. In result blood flow in this vessel was simulated.

1.2 Two-phase hemodynamics

In case of blood flow in microvessels1 it is necessary to use the non-


Newtonian liquid models [2, 47]. It is consequence of the Fahraeus, Fahraeus-
Lindqvist effects and another corresponding features of hemodynamics in mi-
crocirculation.
The appearance of the decreasing of hematocrit in microtubes is described
in [10,20,55]. The decreasing of blood viscosity in case of diameter smaller then
1 mm is described in [2, 14, 30, 31]. The plasma skimming in case of network
bifurcation defines the non-equilibrium hematocrit distribution [2, 47].
Now there are many different researches which admit the construction of
such models. The cellular phase modelling are considered in [15, 35, 46, 58],
for example. There are plasma phase modelling [41], models which are used
interactions cell-to-cell [25, 26], modelling of active and passive regulation in
microvessels [2].
The multiphase hemodynamics models correspond to modelling with cell-
plasma interactions. The main part of cell mass of blood is presented by red
blood cells, so in multiphase hemodynamics the two-phase disperse systems are
used [30, 31, 53, 60]. In these cases the blood is considered as two-phase liquid
with continues layer of plasma and disperse layer of erythrocytes.
In [53] the both phases are considered as Newtonian liquids. Every phase
fills the own volume of the vessel and is described by own stationary Navier–Stokes
equations in cylindrical coordinate system. Plasma fills the cell depleted layer
and erythrocytes are concentrated at central part of vessel. The boundary con-
ditions are added by conjugate conditions, herewith interphase forces are not
1
Radius of vessel must be less then 0.5 mm.

9
considered. The analogy task is presented in [60] but here erythrocyte’s layer
is defined as non-Newtonian liquid with constant viscosity. In both studies it
is considered that the cell depleted layer and hematocrit are depends on vessel
radius.
In [30, 31] a blood plasma fills the entire volume of vessel, the red blood
cells are distributed at vessel with exception of the cell depleted layer. Herewith
the blood viscosity depends on radius of vessel. The motion equations are
equations of inertionless motion of two-phase system with incompressible phases
and constant pressure gradient. The velocities of erythrocytes and plasma are
calculated, it is received that the red blood cells move more quickly than the
blood plasma. The dependence of blood viscosity and hematocrit on vessel
radius is researched. In case of the radius in interval from 5 to 50 µm the
relative viscosity experimental data are bad correlated with model results if
the flow average of hematocrit grows. In other cases the experimental and the
numerical data are well correlated.
The two-phase system without interphase interaction forces is consid-
ered [57] in case of stenosis. The hemodynamic equations are the equations
of magnetohydrodynamics. The influence of temperature is taken into account,
herewith the pressure gradient depends on time according to the harmonic law.
It was interesting the investigation [1] at which a dependence of Reynolds
number from red blood cells was received. In this case a blood flow in micro-
tubes was considered in framework of mixture model [29].
The all above considering multiphase models correspond to hemodynamics
in microvessels. In [5, 16, 21, 33] coronary blood flow simulation was studied.
Herewith four different non-Newtonian viscosity models are compared in case
of two-phase Eulerian–Eulerian method [21,33]. The simulation was performed
for curved coronary artery with the diameter 4,37 mm and the curvature radius
4,15 cm. A pulsatile inlet velocity and an outlet constant pressure were used
for both phases. Moreover, it was received that the mixture viscosity for the

10
two-phase case is some what higher than the single-phase model on the inside
and the outside curvatures. The red blood cells volume fraction is higher on
the inside curvature. The cases with stenosis were not considered. But the
corresponding vessel geometries were considered in [5, 16]. The high and low
hematocrit region were calculated near stenosis but this variation of hematocrit
was sufficiently small.

11
2 Physiological bases of coronary blood flow

2.1 Rheology of blood

Rheological features of blood is based on the such factors as fluidity and


deformability. It is so because blood consists from many different elements:
plasma, red blood cells, white blood cells and other. In this conditions the
blood may be considered as disperse structure.

2.1.1 Basic principles of the theory of disperse system

Disperse system is an union of a disperse and continuous phases. The


disperse phase may consist from the different ”particles” such as powders, gas
bubbles, blood cells. They are distributed over the volume of the liquid and
move with the last. It may be determinated as discrete phase. Herewith the
continuous phase is a basic phase of the disperse media, it is also named as
bearing or liquid phase.

Figure 2.1 — Flow diagram of different disperse structures [3]

Viscosity, fluidity, stability refer to the rheological features of disperse


system [3]. The interactions between the ¡¡particles¿¿ of the discrete phase
define the rheology of the system, see pic. 2.1. At shear motion the differ-
ent layers of liquid may flow with different velocities. In this case as actions
of external forces and intraphase interactions as interphase interactions may

12
significance [37–39, 59].
If particles have spherical shapes or their concentration is small then these
particles move in own layer without moving to a neighboring layers. If particles
have not spherical shapes or their concentration is high then the they get to
neighboring layer. In result, the difference appears between the velocities of the
layers. Additional resistance to movement of layer is consequence the velocity
mismatch. If particles have adhesion to each other they are formed to the stacks
of erythrocytes, rouleaux. This case corresponds to the system with particles
of non-spherical forms.

2.1.2 Blood as a disperse media

Plasma is the main part of the blood (about 60%) and about 99% from
the all blood cells are erythrocytes. So, the blood may be considered as two-
phase disperse medium It must be marked that red blood cells (pic. 2.2) have

Figure 2.2 — Red blood cells. The figure taken from [49]

the shape of a biconcave disk. Its diameter is about 7 − 8 µm, they may
be deformated and coagulated. The flow of erythrocyte through capillaries1
is explained by the erythrocyte ability to deform [12, 45, 52]. The process of
erythrocyte deformation is presented2 on the figure 2.3. On the figure 2.4
receiving in [40] experimental and numerical results3 are presented.
1
The red blood cells is squeezed if they flow through vessels with diametr more smaller than their equilibrium
diametr. For example the capillary diameter my have size about 2-3 microns.
2
The figure taken from publication [52]
3
The figure taken from publication [40]

13
Figure 2.3 — The modelling result of erythrocyte deformation in case of its
flowing through small channel. This confirms that the erythrocyte membrane
bend to a concave form [52]

Figure 2.4 — The experimental results are marked by letter (b) and (e). The
numerical results are marked by another letters

Blood is also characterized by hematocrit, it is a volume ratio of ery-


throcytes in blood. The migration of red blood cells led to formation of a cell
depleted layer near vessel wall. In result the next rheological effects are observed
in vitro and in vivo [9, 10, 14, 30]: the Fahraeus effect, the Fahraeus-Lindqvist
effect, network Fahraeus effect (or plasma skimming).
The Fahraeus effect is the decreasing of ratio Ht /HD in microvessels4 where
Ht is a tube hematocrit and HD is a discharge hematocrit. Let there are two
channels with blood outflow and blood inflow correspondingly, a hematocrit
in these channels is named the discharge hematocrit. It can be calculated by
formula
Z Z
1
HD = Hvds,
Q
S

here Q is a volumetric flow rate, S is an area of vessel cross-section, H is an


erythrocyte concentration and v – blood velocity. It is saw that HD may be
4
The vessels with diameter less than 1 mm.

14
also defined as flow average hematocrit. Let also there is another channel which
connects the above considering channels, a hematocrit in this middle channel
is named the tube hematocrit. It can be calculated by expression
Z Z
1
Ht = Hds,
S
S

it is saw that Ht may be also defined as dynamical hematocrit.


The Fahraeus-Lindqvist effect is a blood apparent viscosity decreases in
the microvessels (d < 1 mm).
The network Fahraeus effect is observed at bifurcation vessels. It is also
named as plasma skimming [47]. At the bifurcation the high flow rate daughter
vessel receives the greater value of hematocrit respect to parent vessel. Here-
with the low flow rate daughter vessel receives the smaller value of hematocrit
correspondingly.

2.2 Functional features of coronary arteries

Arteries consist of three tunicas, see figure 2.5. An internal tunica is named
intima, it contents endothelium cells. An external tunica is named adventitia, it
consists of fibrous connective tissue. A tunica media is a middle layer of vessel,
it consists of muscle and elastic fibers. In different vessels there are various
correlations between muscle and elastic fibers. This defines a building type of
an artery. It may be elastic, muscle or muscular-elastic type [19].
Coronary arteries are arteries covering the heart. They are arteries of
muscle type [19] which bring oxygenated blood to the myocardium. The arteries
locating on the external tissue of the heart are named epicardium arteries.
Herewith the arteries locating on the internal tissue of the heart are named
endocardium or microvascular arteries.
There are two main coronary arteries (see pic. 2.6). The left coronary
artery (LCA) begins at the left aortic sinus. It start from the main stem of the

15
Figure 2.5 — The structure of an artery wall [50]

left coronary artery (LMCA) which is bifurcated5 to the left anterior descending
artery (LAD) and the circumflex artery (Cx).
The right coronary artery (RCA) begins at the right aortic sinus. It goes
to lower part of the heart. RCA ends with the posterior descending artery
(PDA) for more number of patients.
Numerical modelling of coronary blood flow is a non-invasive method for
determination of the cardiovascular system state. One of the reason of coronary
flow injury is a formation of narrowing parts in the arteries. Such part of the
vessel is named as stenosis. Stenotic injuries of the coronary vessels are usually
observed in certain parts of the coronary tree. The LCA stenosis often appear
in the bifurcation region which divided LCA to the left anterior descending
artery and the circumflex artery. The RCA is often narrowed in the proximal
segments [17].
Determination of the hemodynamic significance of the stenosis is provided
by complex of different methods. There are coronary angiography, intravascular
ultrasound, MRI, determination of fractional flow reserve. The last diagnostic
method is based on the calculation of the ratio of maximum blood flow distal
5
Some times there is a trifuracation [36].

16
Figure 2.6 — The coronary arteries tree [32]

to a stenosis to normal maximum flow in the same vessel. As the relationship


between pressure and coronary flow is not linear during basal conditions but it
is linear during maximal coronary hyperemia then the pressure can be measured
instead of the blood flow. Thus
pd
FFR = ,
pn
where pd is the distal pressure measured after the stenosis and pn is the prox-
imal pressure measured before the stenosis, the both pressures are measured
in conditions of maximal hyperemia. The FFR determination is significance
to choose a variant of treatment. For example, in [17] it was be shown that
stenosis with narrowing diameter at 50% to 70% do not require stenting in case
of FFR more than 0.75, a minimal area of lumen more than 4 mm2 and minimal
diameter of lumen more than 2 mm.
There are some problems in FFR determination. One of them consists of
the intravascular measuring of the pressure is the invasive procedure. Another

17
problem appears when there two consequently placed stenosis. It is impossible
to determine which of them is more significance [17]. Sometimes it is enough to
stent only one of the stenosis for hemodynamics improvement. The numerical
simulations can to solve both of them problem.
To correct set boundary conditions for hemodynamics simulation must be
mentioned the following features. The coronary blood flow is defined by vessel
resistance which depends from a changing of intramiocardial and intra-cavity
pressure. At the systole there is a powerful contraction of the left ventricle which
leds to compression of small coronary arteries. As result in the left coronary
artery the blood flow dominates in the diastole phase. In the right coronary
artery the extravessel compression is low and the systolic blood flow is defined
too [17].

18
3 Basics of the multiphase disperse media theory

The different hydrodynamics models [24, 37, 38, 44, 59] are used for blood
flow modelling because the blood is a liquid. The multiphase theory is applied
to describe suspension and emulsion flows [37, 38, 59]. This theory can be con-
sidered in case of hemodynamics modelling as the blood consists of two phases:
plasma and cell component.

3.1 Equations of the multiphase hydrodynamics

The disperse system motion equations are based on the continuity equation

∂ρ
+ div(ρv) = 0
∂t

and Navier-Stokes equation [24]


 
∂v  η
ρ + (v∇) v = −gradp + η4v + ζ + grad(divv).
∂t 3

In case of incompressible viscid fluid1 it is transformed to the next equation [24]

∂v r (v ϕ )2 vr 2 ∂v ϕ
 
r 1 ∂p r
+ (v∇) v − = − + ν 4v − 2 − 2 ,
∂t r ρ ∂r r r ∂ϕ
∂v ϕ ϕ r ϕ r
 
v v 1 ∂p v 2 ∂v
+ (v∇) v ϕ + = − + ν 4v ϕ − 2 + 2 , (3.1)
∂t r ρr ∂ϕ r r ∂ϕ
∂v z 1 ∂p
+ (v∇) v z = − + ν4v z ,
∂t ρ ∂z

which is done in cylindrical coordinate system. Here

v = (v r , v ϕ , v z )

and ρ is a density, p is a blood pressure and a kinematic viscosity ν correlates


with a dynamic viscosity η:
η
ν= .
ρ
1
Here viscosity have a constant value.

19
In cylindrical coordinate system the continuity equation of incompressible viscid
fluid is
1 ∂rv r 1 ∂v ϕ ∂v z
+ + = 0.
r ∂r r ∂ϕ ∂z
For multiphase disperse system the next restrictions [37, 38] are used:
ˆ Every phase occupies the entire volume of space and it is described by the
hydrodynamics equations.
ˆ Phase features (a density, a pressure, a phase energy and other) jump on
the boundary.
ˆ Related equations of system must to take into account phase interactions.
In the multiphase theory a true density2 ρ◦k is a density of the corresponding
phase as a self-contained continuum system. They are related by the expressions
X X
ρ= ρk , ρk = αk ρ◦k , αk = 1 (3.2)
k k

with a density of the all system ρ. Herewith αk is a volume fraction for k-th
phase, ρk is a density for k-th phase.
The velocities are defined by
X
ρv = ρk vk . (3.3)
k

In case of suspension of viscid fluid with particle the viscosity of the system is
defined by Einstein relation [3]

µ = µ1 (1 + C · α2 ),

where µ1 is the viscosity of the continuum phase. The value

µ
η=
µ1

is named as effective viscosity. There are many relations for η calculation. In


case of solid spherical particles C = 2, 5, for ellipsoids C = 5 [37].
2
The low index corresponds to k-th phase. For continuous phase k = 1.

20
In case of collisionless disperse two-phase system there are the next sug-
gestion [37].
ˆ The sizes of inhomogeneities in the mixture are more larger than the sizes
of molecules and less than the distances at which the parameters variations
are significance.
ˆ In every elementary macrovolume the particles of the disperse phase are
spherical and have the same radius.
ˆ Disperse phase volume fraction is very small: α22  1.
ˆ Effects of chaotic and internal movement of the dispersed phase particles
are negleted.
ˆ Direct collisions and processes of the dispersed phase particle coagulation
are neglected too.
Mass equation have the form [37, 38]
∂ρk ∂ρk vki
+ = njmk , (3.4)
∂t ∂xi
∂n ∂nv2i
+ = 0,
∂t ∂xi
here m corresponds to the disperse phase, jmk – velosity of phase transitions in
the direction from m to k. The particle number in a mixture volume unit is
3α2
n=
4πa3
where a is the particle radius.
Let there are no direct interaction between the particles and ρ◦k are con-
stants. Herewith let a pulse of the mixture volume unit equals to the sum of
phase pulses. In these assumptions the phase pulse equations are [37, p. 72]
d1 v 1 ∂σ k1
ρ1 = k
− nf 12 + ρ◦1 α1 g,
dt ∂x
d2 v 2
ρ2 = nf 12 + ρ◦2 α2 g, (3.5)
dt
here
dk v k ∂v k
= + (v k ∇)v k ,
dt ∂t
21
the stress tensor is [37, p. 70]
  
kl Σ
σ1 = − α1 p1 + α2 p2 − 2 δ kl + α2 Πkl + σµkl ,
2a
 
1
σµkl = 2µ ekl − em mδ
kl
, (3.6)
3
1
ekl = ∇k V l + ∇l V k ,

2
V = α1 v1k + α2 v2k ,
k
k l
 
kl ◦ 2 kl w12 w12
Π = −ρ1 (ω1a ) δ +
2
and σµkl is a viscous stress tensor, ekl is a strain tensor, Πkl is a pulse transfer,
a
w12 = v 1 − v2 , ω1a = divV ,
3α2
a is a particle radius, Σ is a coefficient of particle’s surface stress and µ – effec-
tive viscosity defined by Einstein formula. Herewith the interactions between
particles are absent. The particle radius is constant and the phase transmissions
are absent too (jmk = 0).
The interphase interaction force f12 is a sum of the buoyant force fA , the
added mass force fm and the force of viscous friction fµ :

f12 = fA + fm + fµ ,
2πa3 0 d1 v 1 d2 v 2 3 d2 a
 
fm = ρ − + w12 ,
3 1 dt dt a dt
fµ = 6πaµ1 ψa w12 , ψa = α1pw ,

here power pw have a value from 3 to 5 and f12 = −f21 .


Let the interphase interaction force f12 is inserted to the equation (3.5),
then we have
d1 v 1 ∂σ k1
ρ1 = α1 k − α1 nf∗ + ρ◦1 α1 g,
dt ∂x
d2 v 2 ∂σ k1
ρ1 = α2 k + α1 nf∗ + ρ◦2 α2 g, (3.7)
dt ∂x
here
f∗ = fm + fµ

22
and in case of spherical particles

3α2
n= .
4πa3

Take into account that the first term of the right part of the second equa-
tion of (3.7) is the buoyant force.

3.2 Equations of the two-phase hydrodynamics in cylindrical coordinates

As known there are the Navier-Stokes equations in cylindrical coordinate


system [24] but the corresponding equations are not presented in [37] in case of
cylindrical coordinate system. They were not found in another publications.
So we transform the equations (3.4) and (3.7) to cylindrical coordinate
system. For this the Lame coefficients hk are used [24]. In our case

1
h1 = h3 = h1 = h3 = 1, h2 = r, h2 = .
r

In such transformation tensors are not changed by the tensor law in case of
transformation from one curved coordinate system to another.
The gradient operator in cylindrical coordinate system [24] is
 
∂ 1 ∂ ∂
∇= , , , (3.8)
∂r r ∂ϕ ∂z

and the divergence operator is

1 ∂rAr 1 ∂Aϕ ∂Az


divA = + + . (3.9)
r ∂r r ∂ϕ ∂z

We use the formula of the contraction of the tensor derivative which is


presented in [18]. So we have
 
1 1 ∂ √ hm mk 1 ∂lnhk kk
∇k Amk = √ γ A − A , (3.10)
hm γ ∂xk hk hm ∂xm

here γ = (h1 h2 h3 )2 .

23
As result, in the axially symmetric case3 the system’s components not
depend from ϕ so the equations (3.4) are transformed to

∂αk
+ div(αk v k ) = 0. (3.11)
∂t

As in the two-phase case α1 = 1 − α2 we have

∂α1 ∂α2
=− .
∂t ∂t

In result the equation (3.11) goes to

divV = 0. (3.12)

In fist we rewrite the viscous stress tensor σµkl considered in the equation
(3.6) in cylindrical coordinate system. It has the form

2
σµkl = 2µekl − (µ + 2µ1 )divV δ kl , (3.13)
3

where velocity V is determinated in (3.6) and its divergence is defined by re-


lation (3.9). Herewith the strain-displacement tensor ekl can be calculated by
formula
∂V r 1 1 ∂V r ∂V ϕ V ϕ
 
rr rϕ
e = , e = + − ,
∂r 2 r ∂ϕ ∂r r

1 ∂V ϕ V r
 ϕ z ϕ

1 ∂V 1 ∂V V
eϕϕ = + , eϕz = + − , (3.14)
r ∂ϕ r 2 ∂z r ∂ϕ r
z
 z r

∂V 1 ∂V ∂V
ezz = , ezr = + .
∂z 2 ∂r ∂z
Further, taken into account (3.12) we write viscous stress tensor (3.13) as

σµkl = 2µekl . (3.15)

Now, substituting the relation (3.15) to the equation (3.10) we receive the
3
Here k = 1, 2

24
next equalities:

V ϕ ∂µ µ
   
1 ∂V 2 ∂
∇k σµkϕ = 4µ V ϕ + ·∇ µ− + + 2 (µV r ) ,
r ∂ϕ r ∂r r r ∂ϕ

µ ∂V ϕ
 
∂V 1 ∂ µ
∇k σµkr = 4µ V + r
·∇ µ− 2 ϕ
(µV ) − 2 − 2 V r , (3.16)
∂r r ∂ϕ r ∂ϕ r

∇k σµkz = 4µ V z ,

where the operator 4µ is determinated by equation

     
1 ∂ ∂ 1 ∂ ∂ ∂ ∂
4µ = µr + µ + µ (3.17)
r ∂r ∂r r ∂ϕ ∂ϕ ∂z ∂z

herewith

∂V r ∂ 1 ∂V ϕ ∂ ∂V z ∂
   
1 ∂V 1
·∇ = + +
r ∂ϕ r ∂ϕ ∂r r ∂ϕ ∂ϕ ∂ϕ ∂z

and

∂V r ∂ 1 ∂V ϕ ∂ ∂V z ∂
 
∂V
·∇ = + + .
∂r ∂r ∂r r ∂r ∂ϕ ∂r ∂z

Further we assume

∇k α2Πkl = 0


then taken into consideration the relation (3.16) we have that in the cylindrical
coordinate system the equation (3.7) is defined by

   
∂v k divΩ V
ρk + (v k · ∇) v k = −αk ∇p − + 4µ V + ∇ µ −
∂t 2 (3.18)
−αk χ + (−1)k fm + fµ + ρk g k ,


25
where (v k · ∇) is a scalar product of vectors and

Ω = (α2 ρ◦1 w12


r
· w12 , 0, α2 ρ◦1 w12
z
· w12 ) , w12 = v 1 − v 2 , (3.19)
   
1 ∂ ∂ ∂ ∂
4µ = µr + µ , (3.20)
r ∂r ∂r ∂z ∂z
1 ∂  1 ∂ 
divQ = rQ + Q , (3.21)
 r ∂r z ∂z
∂ 1 ∂ ∂
∇= , , , (3.22)
∂r r ∂ϕ ∂z
 
∂Q 1 ∂Q ∂Q ∂Q ∂Qr ∂ ∂Qz ∂
∇Q = ∇, ∇, ∇ , ∇ = + , (3.23)
∂r r ∂ϕ ∂z ∂xi ∂xi ∂r ∂xi ∂z
µ 
r
χ = 2 V , 0, 0 . (3.24)
r

3.3 Mixture model equations

The mixture model equations are the equations which are used in the
Comsol Multiphysics in case of mixture model. These model can be chosen
for two-phase model with continuum and disperse phase. The last may be
presented by liquid droplets, gas bubbles or solid particles. The equations of
the model were considered with the different points of view, the review of the
corresponding methods is presented in [28]. In the Comsol Multiphysics the
next assumption are used.

ˆ The phases densities are sufficient little change.


ˆ Both phases have the same pressure.
ˆ The velocity between the phases is defined in suggestion of a balance be-
tween pressure, viscous and gravity.

The basic theory of the mixture model originates on the two-phase hydrody-
namics equations, see the section 3.1, namely the equations (3.4) and (3.5)
and the above presented theory. The next motion equation of the mixture is

26
received from (3.5) after some transformations, it is
 
∂v α2 ρ2
ρ + ρ(v · ∇)v = −∇p − ∇ · (ρ − α2 ρ2 )vslip vslip +
∂t ρ (3.25)
+∇ · (∇v + ∇v T ) + ρg + F

where
α1 ρ◦1 v1 + α2 ρ◦2 v2
v= ,
ρ
the index 2 corresponds to disperse phase and 1 corresponds to the continuum
phase. Herewith the relations (3.2) and (3.3) were used. The relative velocity
between the phases vslip in the laminar conditions have the form

vslip = v2 − v1 .

The continuity equation in case of mixture is defined by


∂ρ
+ div(ρv) = 0
∂t
and the corresponding equation in the case of disperse phase is
∂α2 ρ◦2
+ div(α2 ρ◦2 v2 ) = 0.
∂t
It must be mentioned that there are some mixture based models which are
characterized by the relative velocity vslip definition. The Schiller-Naumann
and the Hadamard-Rybczynski models are used the next condition
3 C 2 ρ2 ρ − ρ2
|vslip |vslip = − ∇p,
8 a ρ
a is a radius of dispersed phase particles and the drag coefficients C2 in case of
the Schiller-Naumann model and Reynolds number Rep < 1000 is presented by
24
C2 = (1 + 0.15Rep0.687 )
Rep
and in case of Rep > 1000 it equals to constant value Cd = 0.44. Here the
Reynolds number is defined by equation
2aρ1 |vslip |
Rep = .
µ
27
The Hadamard-Rybczynski slip velocity model is valid for Rp < 1, so the drag
coefficient is 2µ1
!
24 1+ 3µ2
C2 = µ1 .
Rep 1 + µ2
Thus it can be received that
µ1
!
2a2 (ρ − ρ2 )µ1 1+ µ2
vslip =− 2µ1 ∇p.
9ρµ 1+ 3µ2

28
4 Two-phase vascular blood flow models

Numerical simulations of hemodynamics were performed by different au-


thors in cases which use the non-Newtonian blood rheology, see for exam-
ple [1, 2, 5, 16, 21, 30]. Some of these models are constructed for microvessels,
another models have various drawbacks in receiving results, see the section 1.2
for more details.
We constructed two models of the two-phase hemodynamics. The first
model is based on the non-stationary equations of collisionless disperse two-
phase system which we transformed to cylindrical coordinate system in the
section 3.2. Analogous equations were used in stationary case by author of
the papers [30, 31]. This model will be presented in the section 4.1. In the
section 4.3 we will present a mixture model of blood flow which is defined
by mixture hemodynamics equations described in [28] and presented in the
section 3.3.
We also constructed a single-phase blood flow model (see the section 4.2)
to compare it with receiving mixture model. Herewith in the final section of
this chapter we discuss the results of numerical simulations.

4.1 Two-phase axially symmetrical collisionless model of hemodynamics

In [30] the two-phase stationary hemodynamics model was received1 for


vessels with diameter less than 1 mm. The two-phase non-stationary model of
hemodynamics is constructed in this study. The next assumptions are used:
ˆ the sizes of inhomogeneities in the mixture are more larger than the sizes
of molecules and less than the distances at which the parameters variations
are significance,
ˆ in every elementary macrovolume the particles of the disperse phase are
spherical and have the same radius,
1
The model depends on the vessel radius and not depends on z and ϕ.

29
ˆ disperse phase volume fraction is very small,
ˆ it is possible to neglect the energy and effects of the chaotic and internal
movement of particles of the disperse phase,
ˆ direct collision and coagulation of the disperse phase particles are not
considered,
ˆ the pressure is is the same in both phases and particle radius is constant,
ˆ the densities ρ◦1 and ρ◦2 are constant too.
For the model construction the assumption

vk = (0, 0, vk (r, t))

is used then the equation system (3.18) goes to


   
∂vk ∂p αk ∂ ∂V α 1 α 2 ∂v 1 ∂v 2
ρk = −αk + µr + (−1)k ρ01 − +
∂t ∂z r ∂r ∂r 2 ∂t ∂t
9 α1 α2
+ (−1)k µ1 ψa (v1 − v2 ), (4.1)
2 a2
∂p ∂V ∂µ
0 = −αk + αk .
∂r ∂r ∂z
If the viscosity not depends from z then the mass equation transforms to the
condition of the pressure independence from radial coordinates.
As known, the blood effective viscosity is calculated by different formu-
las [13], we will use (see [13, 30]) the relation

µ α1−0.8 − 1
η= = 1 + 2.2 . (4.2)
µ1 (1 − 0.45)−0.8 − 1
In this case η(0) = 1.
For numerical simulation the following parameters are used. The plasma
viscosity is
µ1 = 1, 5 · 103 g/(s · mm),

the plasma density corresponds to

ρ◦1 = 1, 03 · 10−3 g/mm3 ,

30
the red blood cells density is

ρ02 = 1, 1 · 10−3 g/mm3 ,

red blood cells radius is a = 4 µm and the pressure is defined by relation

p(t, z) = (1 − 0, 1z)p0 (t)

where

pmax −pmin
p
min + 2 (1 + cos(2πt − π)), t ≤ 0, 7T,
p0 (t) = (4.3)
 pmin , 0, 7T < t ≤ T,

here T = 1 s, pmin corresponds to diastole phase pressure and pmax is a systole


pressure. Herewith pmin = 70 Torr and pmax = 100 Torr and the pressure
gradient is −0, 1p0 (t). The graph of this function is presented on the figure 4.1.

Figure 4.1 — The pressure function using in the simulation

Herewith R = 1, 62 mm is a vessel radius corresponding to a cross sectional


area of LMCA which equals to S = 0, 08 cm2 .
The slip boundary condition on the vessel wall and the zero initial condi-
tions for velocities are used.
It will be considered two different values of hematocrit.

31
4.1.1 The first case of hematocrit function

Let erythrocyte volume fraction2 is defined by relation


 πr 
α2 = 0, 4 cos ,
2R

the corresponding function is presented on the figure 4.2.

Figure 4.2 — The erythrocyte volume fraction in the first case

In this case the numerical simulation results were received, we have that
the velocities of the red blood cells and the plasma are equal.
So the blood velocity V can be calculated from the relation

ρ1 v1 + ρ2 v2
V = .
ρ

Taken into account the equations (3.2) and (3.3) we have that the blood velocity
equals to the plasma and red blood cells velocity, as v1 = v2 . So, the maximum
value of blood velocity is shown at the figure 4.3.
Let us increase the pressure gradient putting now

p = (1 − 0, 2z)p0 (t).
2
It equals to hematocrit.

32
Figure 4.3 — The simulation result for the velocity at the moment t = 0.62T ,
here the period equals to 1 second and p = (1 − 0, 1z)p0 (t). The velocity is
measured in m/s

Figure 4.4 — The velocity at the moment t = 0.62T , here the period T = 1 s
and p = (1 − 0, 2z)p0 (t). The velocity is measured in m/s

33
In this case the blood velocity will increase too. The corresponding results may
be seen at the figure 4.4.
Further consider a volumetric flow rate of blood3 Q, which is
ZR
Q = 2π V (r)rdr.
0

In case of constant blood flux we decrease a radius of the vessel and compare it
with value of the pressure gradient. It was received that the pressure gradient

 − 14
∂p
Figure 4.5 — The ordinate axis shows ∂z , and the abscissa axis shows
the radius of the artery. The pressure is measured in Torr and the radius is
measured in mm. The result was received in case of constant blood flow

is inversely proportional to fourth power of the vessel radius (see figure 4.5):
∂p 1
= .
∂z (1, 09r + 0, 02)4
The absolute error of velocity estimation is about 0,025 m/s.
In the considering case the cell depleted layer was not done by inlet model
parameters and don’t appear as a simulation result. In [30, 31] this layer was
done as inlet function. Thus we do this too in the next construction.
3
It is also named the blood flux.

34
4.1.2 The second case of hematocrit function

Let now erythrocyte volume fraction is a step function



 0, 4 if r ∈ [0, R − h],
α2 = (4.4)
0 if r ∈ (R − h, R].

Here h determinates a thickness of the cell depleted layer. The similar function
was chosen in [30,31] for value of hematocrit too. We also use the next function
for pressure: p = (1 − 0, 2z)p0 (t). The velocity of the plasma v1 is presented on
the figure 4.6. It have the same profile as the erythrocyte velocity v2 and the

Figure 4.6 — The plasma velocity at the moment t = T = 1 s in case of step


function of hematocrit, p = (1 − 0, 2z)p0 (t). The velocity is measured in m/s

blood velocity v which is defined by equation (3.3). The corresponding plots


are done on the figures 4.7 and 4.8.
As you can see, in this case there is a cell depleted layer, its thickness was
fixed by erythrocyte volume fraction. The plasma and RBCs velocity profiles
are similar. Also it was received the difference between plasma and erythrocyte
velocities which is presented on the figure 4.9. It was calculated in region
r ∈ [0, R − h] only4 , because in region r ∈ [R − h, R] the red blood cells velocity
4
Here R is a vessel radius and h is a thickness of cell depleted layer.

35
Figure 4.7 — The red blood cells velocity at the moment t = T = 1 s in case
of step function of hematocrit, p = (1 − 0, 2z)p0 (t)

Figure 4.8 — The blood velocity at the moment t = T = 1 s in case of step


function of hematocrit, p = (1 − 0, 2z)p0 (t)

equals to zero. It is seen that the velocity profile is different from Poiseuille
profile.
In this simulation the dependence of hematocrit and viscosity on vessel
radius is a constructive feature of the model. All known multiphase blood
flow simulations use different rheological models for viscosity determination.
In our case the blood viscosity is described by Einstein equation with specific
parameters which were suggested in [30, 31]. Our results are coordinated with

36
Figure 4.9 — The difference v2 − v1 in m/s, at the moment t = T = 1 s and in
case of step function of hematocrit, p = (1 − 0, 2z)p0 (t). Here v2 is RBCs
velocity and v1 is plasma velocity

results of other authors [30, 31, 47, 53, 60] in that the hematocrit and viscosity
are depend on vessel radius. In the studies of author [30,31] there is a difference
between plasma and erythrocytes velocities. In our model these velocities do
not differ in case of first hematocrit function and very small differ in case of step
hematocrit function. This difference is about 7-8 RBC diameter per second.
The principle feature of the constructed model consists in the using of
non-stationary equations and a pulse wave. Herewith the results were received
not for small vessels. The authors [30, 31, 47, 53, 60] considered the stationary
blood flow.

4.2 Single-phase laminar blood flow

The single-phase simulation were provided to compare these results with


two-phase modeling which will present further. Corresponding flow is described

37
by Navier-Stocks equations (3.1) above presented. Calculations were received
in Comsol Multiphisics.
The rigid vessel with radius 1.62 mm and length 10 mm is constructed in
axially symmetric geometry. The initial values are

v r = 0, m/s v z = 0, 2 m/s

and pressure equals to pmin in case of z < 1 and p = 0 in other cases.

Figure 4.10 — The pressure function using in the simulation at the inlet

Inlet flow is defined by p(t) = p0 (t) where p0 is described by (4.3) with


pmin = 60 and pmax = 110, see figure 4.10. Herewith the viscous stress vanishes
in this boundary.
Outflow corresponds to normal mixture velocity field vout (t) interpolated [48]
from the discrete values, the corresponding function presented at the figure 4.11.
At the vessel wall there is a no slip condition. Herewith fluid properties
are
ρ = α2 ρ◦2 + α1 ρ◦1

where
ρ◦1 = 1, 03 · 10−3 g/mm3

38
Figure 4.11 — The ordinate axis shows vout (t) in m/s, and the abciiss axis
shows the time in seconds

is the plasma density and the red blood cells density is

ρ02 = 1, 1 · 10−3 g/mm3 ,

the blood viscosity µ is defined by (4.2) with

µ1 = 1, 5 · 103 g/(s · mm)

and hematocrit equals to 0.4. The red blood cells radius is a = 4 µm.

Figure 4.12 — The pressure of the single-phase laminar flow in the rigid vessel

It was received that the pressure is the same at all points of the vessel,
corresponding time dependence is done on the figure 4.12. The velocity has a

39
Figure 4.13 — The velocity of the single-phase laminar flow in the rigid vessel,
it is time dependence

radial distribution (see pic. 4.14) and ts time dependence is presented on the
figure 4.13.
Now we construct a two-phase model of hemodynamics.

4.3 Two-phase mixture model

Let us consider the equations of mixture model (3.25), the gravity force ρg
and the added force F are not taken into account. The numerical simulations
based on the mixture model will be performed in the Comsol Multiphysics.
The two-phase simulation in the same rigid vessel as in the single-phase
case was realized in the Comsol Multiphysics. So, in new conditions, the model
equations consist from the motion equations
 
dv α2 ρ2
ρ = −∇p − ∇ · (ρ − α2 ρ2 )vslip vslip + ∇ · (∇v + ∇v T ) (4.5)
dt ρ

and the continuity equations for the mixture and the disperse phase
∂ρ
+ div(ρv) = 0,
∂t (4.6)
∂α2 ρ◦2
+ div(α2 ρ◦2 v2 ) = 0.
∂t
40
Figure 4.14 — The velocity of the single-phase laminar flow in the rigid vessel,
the vertical axis shows v(t) in m/s, at t = 1 s

Herewith in equation (4.5) is used the next derivative

dv ∂v
= + (v · ∇)v.
dt ∂t

For more details see the section 3.3.


The boundary and the initial conditions are the same as in the single
phase case. The analogous conditions appear for the disperse phase. It must
take into account that the initial distribution of the disperse volume fraction is
equal everywhere.
Inlet flow is defined by pressure (4.3) with vanishing viscous stress of mix-
ture. At the diastole pressure equals to pmin = 60 Torr and at the systole
pmax = 110 Torr. Disperse phase volume fraction equals to α2 = 0.4 every-
where.
Outflow corresponds to normal mixture velocity field vout (t), see the fig-
ure 4.11. Disperse phase volume fraction equals to α2 = 0.4 too.
At the vessel wall there is a no slip condition. Disperse phase volume
fraction equals to zero.

41
The mixture model requires to choose a slip velocity determination (see the
section 4.5). We use the Hadamard-Rubczynski slip model for liquid droplets
or bubbles:
µ1
!
2a2 (ρ − ρ2 )µ1 1+ µ2
vslip =− 2µ1 ∇p.
9ρµ 1+ 3µ2

Thus we assume that the plasma viscosity

µ1 = 1, 5 · 103 g/(s · mm)

and the red blood cells viscosity is defined by relation µ2 = 1, 5µ1 , we used the
study [54] for RBCs viscosity estimation. The plasma density ρ◦1 and the red
blood cells density ρ02 are the same as at the above considered models.
These model conditions are identical for case of normal and stenotic vessels.
The models are different not only by geometry. The viscosity construction will
be calculated by different ways too.
In first, consider a case of normal vessel.

4.3.1 Numerical simulation in case of normal vessels

The blood viscosity is defined by expression (4.2) everywhere, herewith


the value of α2 not determinated. As viscosity as hematocrit are calculated as
solutions of the model.
The next results were received. The mixture velocity is presented on the
figure 4.15 at time 0, 62 s. Its time dependence is done on the figure 4.16 at the
point r = 0 mm and z = 5 mm. At the time t = 0, 62 second we also plotted
the RBCs velocity at the figure 4.17. Comparing the figures 4.15 and 4.17 the
difference between these velocities can not be found visually. It is seen that
a minimal value of the mixture velocity equals to zero opposite to a minimal
value of the erythrocytes velocity which has an order of about 40 micrometers
per second. To estimate the difference between these velocities we ploted a slip
velocity vslip at the figure 4.18. As you can see it has an order about 10−7 m/s.

42
Figure 4.15 — The mixture velocity of the two-phase laminar flow in the rigid
vessel, the vertical axis shows v in m/s at the time t = 0, 62 s

Figure 4.16 — The time dependence of the mixture velocity of the two-phase
laminar flow in the rigid vessel, the vertical axis shows v(t) in m/s at the
point with r = 0 and z = 5 mm

43
Figure 4.17 — The red blood cells velocity of the two-phase laminar flow in
the rigid vessel, the vertical axis shows v2 in m/s at time 0, 62 s

Comparing the slip velocity with RBC diameter we receive that erythrocytes
move faster than plasma by 2-3 own diameters per second. It is three to four
times less than in the previous collisionless two-phase model.
At the figure 4.19 you can see a pressure dependence on z-coordinate.
Obviously, the difference between the pressure around the vessel axis and the
pressure near the vessel wall appears due to boundary condition influence. The
last one would end on 2 mm after the inlet and before the outlet of the vessel.
So it can be concluded that the pressure does not depend on vessel radius in
the region of vanishing influence of boundary conditions. The pressure gradient
in this vessel part equals to value about 0,03 Torr/mm.
It must be marked, a time-dependence of the pressure is done on the
figure 4.20. Its time profile corresponds to the using inlet pulse wave.
As a result of the simulation a RBCs volume fraction was received too.
The hematocrit small depends on time and depends on the vessel radius, see
figures 4.21–4.23. Near the vessel wall a minimal erythrocytes volume fraction
takes place at the peak of the blood flow velocity, see figures 4.16 and 4.23.
Herewith at the vessel axis a hematocrit has minimum a little before the time

44
Figure 4.18 — The slip velocity between RBCs and plasma in case of the
two-phase laminar flow in the rigid vessel, the vertical axis shows vslip in m/s
at the point r = 0 and z about 5 mm

Figure 4.19 — Pressure dependence on z is presented at a systole

45
Figure 4.20 — The pressure at the point r = 0 and z about 5 mm

Figure 4.21 — The RBCs volume fraction at the point r = 0 and z ≈ 5 mm

at which it appears near the wall. This moment corresponds to the beginning
of a systole.
At the period about 0,8-0,9 seconds an increasing of the slip velocity leads
to a decreasing of the RBCs volume fraction at the center of vessel, see fig-
ures 4.18 and 4.22. It is apparent. If particles velocity is growing relative
to plasma flow then number of particles per unit volume drops. Taking into
consideration the plot 4.20 we can conclude that a pressure boost leads to an
increasing of the RBCs volume fraction at the vessel axis and only after this its
growth appears near the vessel wall.
Considering presented on the figure 4.24 plot we can see an appearance of

46
Figure 4.22 — The RBCs volume fraction at the point r = 0 and z about 5
mm

Figure 4.23 — The RBCs volume fraction at the point r = 1, 5 mm and z


about 5 mm

Figure 4.24 — The RBCs distribution in case of laminar flow near the wall.
There is a cell depleted layer

47
a cell depleted layer. It is so despite constant hematocrit at the beginning, see
figure 4.24. At a distance of 20 micrometers from the vessel wall a hematocrit
has a value about 0,25 but at a distance of 10 micrometers from the vessel wall
it drops twice.
Now we include a stenosis to the considering vessel.

4.3.2 Numerical simulation in case of stenotic vessels

There are two types of stenotic wall was constructed. They are presented
at the figures 4.25 and 4.26. The vessel radius equals to 1,62 mm too.

Figure 4.25 — The stenotic Figure 4.26 — The stenotic


vessel in one case vessel at the case

A degree of the first stenosis (see pic. 4.25) is about 31% and a degree of
the second stenosis is about 49% (see pic. 4.26).
These simulations differ from the case of normal vessel by blood viscosity
determination. In this case we admit that µ is defined by (4.2) in points with
r < 0, 9R, where R is the vessel radius. For other values of radial coordinate
we have µ = µ1 where µ1 = 1, 5 · 103 g/mm3 . Herewith α1 equals to 0.6 The
erythrocyte distribution is calculated at the model too.

48
The boundary and initial conditions are described above in this section.
In first we describe a pressure which was calculated for both stenotic ves-
sels. A diastolic pressure is presented on the figures 4.27 and 4.28. A receiving

Figure 4.27 — The pressure at Figure 4.28 — The pressure at


the diastole, it is 31% stenosis the diastole, it is 49% stenosis

systolic pressure you can see on the figures 4.29 and 4.30 correspondingly. To
note, the high pressure zones at the ends of the vessels appear due to boundary
conditions and ones must be ignored.
As you can see, a decreasing of pressure behind stenosis is more significant
in a vessel with a greater degree of narrowing.
At the figure 4.31 a time dependence of a pressure is ploted for both cases of
stenosis at the point r = 0 and z = 5 mm, it corresponds to center of stenosis.
Blue line corresponds to a stenotic vessel with degree of narrow about 31%,
and a red line corresponds to a stenosis of 49% degree of narrow. Comparing
the both curves we can conclude that a diastole phase lengthens as the vessel
narrows.
Receiving values of the mixture velocities are presented on the figures 4.32

49
Figure 4.29 — A systolic Figure 4.30 — A systolic
pressure in case of 31% stenosis pressure in case of 49% stenosis

Figure 4.31 — A systolic preassure for 31% stenosis and 49% stenosis

and 4.33 correspondingly. Its time dependence you can see at the figures 4.34
and 4.35. The blue and red lines on these plots determinate the mixture
velocities at the vessel axis before stenosis and at the points of maximum vessel
narrowing. The green and yellow lines correspond to these velocities at the
vessel axis too but only behind the stenosis.

The mixture velocities distribution on radial coordinate is done at the

50
Figure 4.32 — The velocity at Figure 4.33 — The velocity at
the 31% stenosis is done in the 49% stenosis is done in
mm/s mm/s

figures 4.36 and 4.37. The yellow lines determinate it at the vessel axis in the
center of stenosis. As you can see, these values drop sharply to zero near the
stenotic wall.
To compare RBCs and plasma velocities we constructed plots of slip ve-
locities which are presented at the figures 4.38 and 4.39. As you can see, the
slip velocity at the figure 4.39 is greater then one at the figure 4.38. The order
of these values is comparable to the erythrocytes diameter.
It is not hard to notice, there is a small peak of the mixture velocity behind
the stenosis near the wall, see figures 4.36 and 4.37. This is due to a specific
red blood cells distribution which is presented at the figure 4.40 for the 31%
stenosis and at the figure 4.41 for the 49% stenosis too.
We can see that a cell depleted layer is appear as in above considering
cases, see figure 4.42. Behind stenosis it have a more complex structure then
before stenosis.

51
Figure 4.34 — The velocity at the 31% stenosis is done about the vessel center

Herewith behind stenosis the low hematocrit layer is appeared and it de-
creases when removed from the stenotic part of vessel. But in this layer there
is a high RBCs volume fraction zone, see figures 4.43 and 4.44.

4.4 Comparative analysis of the numerical simulations

In this study the two-phase hemodynamics models were constructed. One


of them is a two-phase non-stationary axially symmetrical collisionless model of
hemodynamics based on the equations of a two-phase collisionless hydrodynam-
ics [37, 38]. These equation were transformed to cylindrical coordinate system
in this study because they were found in Cartesian coordinate system only in
other literature.
A disadvantage of the model consists in simplification. In this case it was
assumed that velocity depends on radius but not depends on z. It is due to
features of the implementation of the finite element method using in Comsol
Multiphysics which have restrictions on boundary and initial conditions setting.
The model requires a refinement. May be, it is possible to create another imple-
mentation of the finite element method by using some programming language.
Despite simplified implementation, some results consistent with studies of other
authors were obtained. For example, in case of second RBCs volume fraction

52
Figure 4.35 — The velocity at the 49% stenosis is done about the vessel center

Figure 4.36 — The velocity at the 31% stenosis depends on r

Figure 4.37 — The velocity at the 49% stenosis depends on r

53
Figure 4.38 — It is a slip velocity dependence on r for the 31% stenosis

Figure 4.39 — It is a slip velocity dependence on r for the 49% stenosis

using, receiving blood velocity profile is simple to corresponding velocity profile


which was calculated in [30, 31]. Herewith it was received that erythrocytes
move little faster then plasma. It is the same result as presented in [30, 31]
too. But the corresponding slip velocity is comparable to value of several red
blood cell diameters per second. So this may be ignored in further numerical
simulations.

An advantage of this model consists in using of time-dependence pressure


gradient, corresponding model was constructed only in stationary case by au-
thor of the articles [30, 31]. A cell depleted layer appears in this model too (see

54
Figure 4.40 — It is a volume fraction of red blood cells at the 31% stenosis

Figure 4.41 — It is a volume fraction of red blood cells at the 49% stenosis

also [9, 30, 31, 53, 60]).


For further investigations it is planed to receive an implementation of
model on some programming language by the finite element method. This
model has a limited use.
The second constructed model is devoid of the shortcomings of the previous
simulation. It is a two-phase axially symmetrical model based on the mixture
model equations.
The advantage of this model consists in the appearance of the cell depleted
layer (or hematocrit) which is a solution of numerical calculations. In other

55
Figure 4.42 — There are cell depleted layers, results is done at points behind
stenosis

Figure 4.43 — RBCs volume fraction (or hematocrit) dependence on r for the
31% stenosis

Figure 4.44 — RBCs volume fraction (or hematocrit) dependence on r for the
49% stenosis

56
publications (see for example [9, 30, 31, 53, 60]) the cell depleted layer is defined
by some function. At this model the hematocrit was done only at the inlet and
outlet boundary. The influence of these boundary conditions is vanished on the
some distance from the boundaries. The initial conditions not influence on the
solution after one period of pulse wave too.
At the all known articles the RBC distribution is a some function of the
model. Our result shows that the cell depleted layer appears as a result of inter-
phase interactions. The RBC distribution is calculated during the simulation.

Figure 4.45 — The red blood cells distribution in case of second stenosis. The
zone of high hematocrit near the wall. Time of 0.62 of period

The next important result is hematocrit distribution after the stenosis. It


was received that there is a region of the hematocrit growing near the wall after
stenosis. Location of the area after stenotic injury with increased red blood cell
emergence near the vessel wall depends on the atherosclerosis degree. At the
figure 4.40 a zone of high hematocrit is placed near the stenosis and have the
RBC volume fraction about 0,4-0,5.
On the figure 4.45 the corresponding zone is placed more far at stenosis
and hematocrit at these zone is about 0,6-1.
Moreover, at the systole phase the high RBC zone is more far from stenosis

57
Figure 4.46 — The red blood cells distribution in case of second stenosis. The
zone of high hematocrit near the wall. Time of 0.68 of period

Figure 4.47 — The red blood cells distribution in case of second stenosis. The
zone of high hematocrit near the wall. Time of 0.78 of period

then at other times. See figures 4.45 – 4.47. When pressure is decreased the
high RBC zone grows away from stenosis.

These RBC distribution may appear because of there is a central blood


flow with high velocity. Some red blood cells can to come off the main flow. In
this case RBCs will go around in these region. Getting out of the high RBC
zone will be difficult due to high velocity of the central blood flow. As result

58
the red blood cells can accumulate in the zone.
These result requires clarification and further research because of this effect
may be a consequence of inappropriate mesh choosing during a simulation.
Despite this, the study [66] should be considered in the context of the
our results. An in vitro investigation of a dynamics of mixture of platelet-
sized fluorescent particles and RBC suspension was studied. A narrowing glass
microchannel was constructed. The dynamics of the receiving particles mixture
in this microchannel was investigated. It was received that there is a high
platelet-sized particles zone which is located several microns away from the
wall. Moreover in the cell depleted layer RBCs recirculate and confluent to the
main flow. It is consistent with our results.
Also in the study [66] was received that before or behind narrow part of
microchannel the cell depleted zone appear too. I our study there is a little cell
depleted zone in considering parts of stenosis.
Thus our results are consistent with both theoretical studies and experi-
mental ones.

59
CONCLUSION

During the study all planed tasks were solved. As a consequence the
following results were obtained:
ˆ rheological properties of blood and basic features of the theory of multi-
phase disperse systems were studied;
ˆ two-phase collisionless hemodynamic equations in cylindricaly-symmetric
coordinate system were received;
ˆ an axially-symmetric collisionless model of two-phase hemodynamics was
constructed;
ˆ an axially-symmetric mixture model of two-phase blood flow and a single
phase hemodynamics model were constructed in Comsol Multiphysics;
ˆ axially-symmetric mixture model was adapted to numerical simulation of
blood flow in stenotic vessels in Comsol Multiphysics.
Using of rheological properties of blood to provide a numerical simulations
of blood flow is a perspective direction in modern studies. In case of different
models of microcirculation this approach is widely adopted. But insufficient
number of studies are used features of blood rheology in case of big vessel.
More over the corresponding approach is used in few cases only.
During this investigation the basic features of the theory of multiphase
hydrodynamics were studied. Receiving two-phase collisionless hemodynamic
equations in cylindricaly-symmetric coordinate system was adopted to construct
a collisionless axially-symmetric model of two-phase hemodynamics. A numer-
ical simulation was performed in Comsol Multiphysics. The main results cor-
responds to other researchers but a difference of this model consists in using
of time-dependent calculations. There is a disadvantage of the result which
consists in suggestion that velocity not depends on z-coordinate. We assume
the next development of constructing model.
The next receiving model is an axially symmetrical 2d mixture model. We

60
adapted these equations to construct of the corresponding model which describe
the blood flow in arteries. The simulations were done in Comsol Multiphysics
too as in normal as in stenotic vessels. It was shown that
ˆ a volume fraction of the RBCs depends on radius and a geometry of vessel
and small depends on the initial and boundary distribution,
ˆ a cell depleted layer appear near the vessel wall and near a stenosis,
ˆ there is a high hematocrit zone in region behind stenosis.
In common all results are agreement with data obtained by other authors.
The result about the existence of a high hematocrit zone was not found in
literature. We think that the high hematocrit zone can influence to the progress
of the stenotic injury. This result requires clarification and further research. For
this investigation it is necessary to take into account the elastic properties of
the vascular wall.
The results of the study were reported and discussed at the scientific sem-
inars of the General and experimental physics department of TSU.

61
REFERENCES

1. A numerical study of blood flow using mixture theory / Wu W. [et al] //


International Journal of Engineering Science. – 2014. – Vol. 76. – P. 56-72.

2. Arciero Z.C. Mathematical methods for modeling the microcirculation /


J.C. Arciero, P. Causin , F. Malgaroli // Biophysics. – 2017. – Vol.4. –
P.362-399.

3. Bibik E.E. Rheology of Disperse Systems / E.E. Bibik. Leningrad:


Leningr. Gos. Univ., 1981.

4. Blood flow dynamics and fluid–structure interaction in patient-specific bi-


furcating cerebral aneurysms / A. Valencia [et al] // International Journal
for Numerical Methods in Fluids. – 2008. – Vol. 58. – P. 1081-1100.

5. Buradi A. Effect of stenosis severity on shear-induced diffusion of red blood


cells in coronary arteries / Journal of Mechanics in Medicine and Biology.
– 2019. – Vol. 19, No. 5. – 1950034

6. Chaichana T. Computation of hemodynamics in the left coronary artery


with variable angulations / T. Chaichana, Z. Sun, J. Jewkes // Journal of
Biomechanics. – 2011. – Vol. 44. – P. 1869–1878

7. Cox R.H. Wave propagation through a newtonian fluid contained within


a thick-walled viscoelastic tube // Biophys. J. – 1968. – Vol.8. P.691–709.

8. Dobroserdova T.K. Numerical simulation of blood flow at presence of vas-


cular implants or pathologies: diss. . . . cand. phys.-math. sciences/ T.K.
Dobroserdova. – Moskow, 2013. – 102 p.

9. Experimental and numerical study o blood flow in µ-vessels: influence of


the Fahraeus-Lindqvist effect /Y.G. Stergiou [et al] // Fluids. – 2019. –
Vol. 4. – P. 143-159
10. Fahraeus R. The viscosity of the blood in narrow capillary tubes/ R.
Fahraeus, T. Lindqvist // American Journal of Physiology-Legacy Con-
tent. – 1931. – Vol.96. P. 562-568.

11. Frank O. The basic shape of the arterial pulse. First treatise: mathematical
analysis.// Journal of Molecular and Cellular Cardiology. — 1990. — Vol.
22, iss. 3. — P. 255–277.

12. Freund J. B. The flow of red blood cells through a narrow spleen-like slit
// Phys. Fluids. – 2013. – Vol.25. – 110807

13. Georgievskii D. V. Efficient yield limit in constitutive correlation of blood


in vivo // Vestnik Moskov. Univ. Ser. 1. Mat. Mekh. – 2006. – Vol. 5. –
P.51–54

14. Gould I.G. Hematocrit distribution and tissue oxygenation in large micro-
circulatory networks / I.G. Gould, A.A. Linninger // Microcirculation. –
2015. – Vol. 22. P. 1-18

15. Hariprasad D.S. Two-dimensional simulation of red blood cell motion near
a wall under a lateral force / D.S. Hariprasad, T.W. Secomb // Phys. Rev.
E Stat. – Nonlin Soft. Matter. Phys. – 2014. – Vol.90. – 053014.

16. Huang J. Pulsatile flow in a coronary artery using multiphase kinetic the-
ory / J. Huang, R. W. Lyczkowski, D. Gidaspow // Journal of Biome-
chanics. – 2009. – Vol. 42. – P. 743-754

17. Ivanov V.A. Intravascular Intravascular research methods in interven-


tional cardiology / V. A. Ivanov, M. J. Movsesyanc, I. V. Trunin – M.
: Medpractice-M, 2008. – 268 p.

18. Kamenkovich V.M. Tensor analysis of main differential operators of hydro-


dynamics of ocean movements in orthogonal curvilinear coordinate system
/ V.M. Kamenkovich, D.A. Nechaev// Oceanological research. – 2019. –
Vol. 47, ›2. – P.139-171.

63
19. Kayumov F.A. Cardiovascular system. Its importance for surgical practice:
student tutorial / F.A. Kayumov, M.A. Nartaylakov, Ufa: Publishing of
Bashkir State Medical University, 2013. – 69 p.

20. Kim S. The cell-free layer in microvascular blood flow / S. Kim [et al] //
Biorheology. – 2009. – Vol.46. P. 181-189.

21. Kim Y.H. Multiphase non-Newtonian effects on pulsatile hemodynamics in


a coronary artery /Y.H. Kim, P.J. VandeVord, J.S. Lee // Int. J. Numer.
Meth. Fluids. – 2008. – Vol. 58. – P. 803–825.

22. Kokalari I. Review on lumped parameter method for modeling the blood
flow in systemic arteries / I. Kokalari, T. Karaja, M. Guerrisi // J. Biomed-
ical Science and Engineering. – 2013. – V. 6. – P. 92-99.

23. Kornelik S.E. Calculation hemodynamics / S.E. Kornelik, A.M.


Bubenchikov, Tomsk: TSU, 2003. – 412 p.

24. Landau L. D. Fluid Mechanics. Vol. 6 / L. D. Landau , E. M. Lifshitz, M.:


Nauka, 1987.

25. Liu Y. Coupling of Navier-Stokes equations with protein molecular dy-


namics and its application to hemodynamics./ Y. Liu [et al] // Int. J.
Numer. Meth. Fluids. – 2004. – Vol.46. – P. 1237-1252.

26. Liu Y. Rheology of red blood cell aggregation by computer simulation.


/Y. Liu , W.K. Liu // J. Comput. Phys. – 2006. – Vol.220. – P. 139–154.

27. Lumped parameter model for hemodynamic simulation of congenital heart


diseases. / S. Shimizu [et al] // J. Physiol. Sci. – 2018. – Vol. 68. – P. 103-
111.

28. Manninen M. On the mixture model for multiphase flow / M. Manninen,


V. Taivassalo, S. Kallio // VTT Publications. – 1996. – Vol.288. – P. 3-67

29. Massoudi M. Modeling and numerical simulation of blood flow using the
theory of interacting continua. / M. Massoudi, J. Kim, J.F. Antaki //

64
International Journal of Non-Linear Mechanics. – 2012. – Vol. 47. – P.
506-520.

30. Medvedev A.E. Two-phase blood flow model in large and small blood
vessels // Mathematical biology and bioinformatics. – 2011. – Vol.6, ›2.
P.228-249

31. Medvedev A.E. Empirical two-phase model of blood flow in vessels less
than 1000 microns // The XI All-Russian Congress on Fundamental Prob-
lems of Theoretical and Applied Mechanics”, Uchenye Zapiski Kazanskogo
Universiteta. Seriya Fiziko-Matematicheskie Nauki, V.157, no. 3, Kazan
University, Kazan, 2015, P.2515-2517.

32. Moorjani N. Key Questions in Cardiac Surgery: Translation from English


edited by academician of the Russian Academy of Sciences Yu.V. Belov /
N Moorjani. N Viola. SK Ohri, M.: GEOTAR-Media, 2021.

33. Multiphase hemodynamic simulation of pulsatile flowin a coronary artery


/ J. Jung [et al] // Journal of Biomechanics. – 2006. – Vol. 39. – P. 2064-
2073

34. Mynard J. P. A 1D arterial blood flow model incorporating ven tricular


pressure, aortic valve and regional coronary flow using the locally con-
98 servative Galerkin (LCG) method / J. P. Mynard, P. Nithiarasu //
Communications in numerical methods in engineering. – 2008. – Vol. 24.
– P. 367–417.

35. Nakamura M. Spring-network-based model of a red blood cell for simulat-


ing mesoscopic blood flow / M. Nakamura, S. Bessho, S. Wada // Int. J.
Numer. Method Biomed. Eng. 2013. – V. 29. – P.114-128

36. Nekrasov A.S. Successful endovascular treatment for LCA trunk trifurca-
tion lesion / A.S. Nekrasov, A.A. Grechishkin, S.V. Mayngart // Innova-
tive medicine of Kuban – 2017. – Vol.2. – P.28-33.

65
37. Nigmatulin R.I. Dynamics of multiphase media, V. I/ R.I. Nigmatulin –
M.: Nauka, 1987

38. Nigmatulin R.I. Dynamics of multiphase media V. II / R.I. Nigmatulin –


M.: Nauka, 1987

39. Nigmatulin R.I. Fundamentals of mechanics of heterogeneous media / R.I.


Nigmatulin – M: Nauka, 1978.– 336p.

40. Numerical-experimental observation of shape bistability of red blood cells


flowing in a microchannel / A. Guckenberger [et. al.] //Soft Matter. –
2018. – Vol.14. – P.2032-2043

41. Numerical methods for simulating blood flow at macro, micro, and multi
scales/ Y. Imai [et al] // J. Biomech. – 2016. – Vol.49. – P.2221–2228.

42. One-dimensional modeling of vascular network in space-time variables /


S. J. Sherwin [et. al.] // J. of Engineering Mathematics. – 2003. – Vol. 47.
– P. 217–250.

43. Patient-Specific Modeling of Blood Flow and Pressure in Human Coronary


Arteries / H.J. Kim [et. al.] // Annals of Biomedical Engineering. – 2010.
– Vol. 38, No. 10. – P. 3195–3209

44. Pedley T. J. The fluid mechanics of large blood vessels /T.J. Pedley –
Cambridge: Cambridge University Press, 1980.

45. Picot J. A biomimetic microfluidic chip to study the circulation and me-
chanical retention of red blood cells in the spleen /J. Picot [et al] // Am.
J. Hematol. – 2015. Vol.90. – 339

46. Pozrikidis C. Numerical simulation of the flow-induced deformation of red


blood cells. // Ann. Biomed. Eng. – 2003. Vol. 31. – P.1194–1205.

47. Pries A.R. Generalization of the Fahraeus principle for microvessel net-
works / A.R. Pries, K. Ley, and P. Gaehtgens // American Journal of

66
Physiology-Heart and Circulatory Physiology. – 1986. Vol.251, N.6, P.
H1324-H1332

48. Razavi S.E.,Omidi A.A., Zanjani M.S. Numerical investigation of blood


flow in a deformable coronary bifurcation and non-planar branch /S.E.
Razavi , A.A. Omidi, M.S. Zanjani // BioImpacts. – 2014. Vol.4. P.199-
204

49. Renal hematuria: the cause of blood in the urine needs to be clarified [Elec-
tronic resource] //Medical atlas. – URL: https://med-atlas.ru/vnutrennie-
organy/gematuriya-chto-eto-takoe.html (access date: 17.05.2021).

50. Rogers D., Lowe S. Ultrastructure of Blood Vessels [Electronic


resource]/ D. Rogers, S. Lowe // TeachMe Anatomy. – URL:
https://teachmeanatomy.info/the-basics/ultrastructure/blood-vessels/
(access date: 17.05.2021).

51. Sajith Kumar K. K. Simulation of Human Cardiovascular System: dis.


degree of Master of Technology/K. K. Sajith Kumar. – Rourkela: National
Institute of Technology Rourkela, 1995. – 61 p.

52. Salehyar S. Deformation and internal stress in a red blood cell as it is


driven through a slit by an incoming flow/ S. Salehyar, Q. Zhu // Soft.
Matter. – 2016. – Vol. 12. – P. 3156-3164

53. Sharan M. A two-phase model for flow of blood in narrow tubes with
increased effective viscosity near the wall /M. Sharan , A.S. Popel //
Biorheology. – 2001. – Vol. 38. – P. 15-428.

54. Snegireva L.V. Rheological properties of erythrocytes in their ontogenesis


/ L.V. Snegireva, V.P. Ivanov // Kursk Scientific and Practical Bulletin
”Man and His Health”. – 2007. – N.1. – P.35-44.

55. Sriram K. Non-Newtonian flow of blood in arterioles: consequences for wall


shear stress measurements / K. Sriram, M. Intaglietta, D.M. Tartacovsky

67
// Microcirculation. – 2014. – Vol. 21. – P. 628-639

56. Sutera S. P. The History of Poiseuille’s Law /S. P. Sutera, R. Skalak R.


// Annual Review of Fluid Mechanics. – 1993. – Vol.25. P.1–19.

57. Tripathi B. MHD pulsatile two-phase blood flow through a stenosed artery
with heat and mass transfer [Electronic resource]/ B. Tripathi, B.K.
Sharma, M. Sharma //arXivLabs, URL:https://arxiv.org/abs/1705.09794
(access date: 17.05.2021)

58. Tsubota K. Effect of the natural state of an elastic cellular membrane on


tank-treading and tumbling motions of a single red blood cells – A review
/ K. Tsubota, S. Wada // Phys. Rev. E Stat. Nonlin. Soft Matter Phys.
– 2010. – Vol. 81. – 011910

59. Velikanova J.V. Hydromechanics of multiphase media /J.V. Velikanova, –


Samara: SSTU, 2009.

60. Verma S.R., Srivastava A., Analitical study of a two-phase model for
steady flow of blood in a circular tube /S.R. Verma, A. Srivastava //
Int. Journal of Engineering Research and Applications. – 2014. – Vol.4,
›12. – P.1-10.

61. Volarovich M. P. Poiseuil’s work on the flow of liquid in pipes (To the
centenary since publication) // Izzvestiya Acad. Sci. USSR, Physics Series.
– 1947. – Vol. 11, › 1.

62. Womersley J.R. Method for the calculation of velocity, rate of flow and vis-
cous drag in arteries when the pressure gradient is known // J. Physiology.
– 1955. – Vol.127, N3. P. 553–563.

63. Womersley J. R. Oscillatory flow in arteries: the constrained elastic tube


as a model of arterial flow and pulse transmission // Physics in Medicine
and Biology. – 1957. – Vol . 2. P. 178–187.

68
64. Womersley J. R. Oscillatory flow in arteries II: the reflection of the pulse
wave at junctions and rigid inserts in the arterial system // Physics in
Medicine andBiology. – 1958. – V. 2. P. 313–323.

65. Womersley J. R. Oscillatory flow in arteries III: flow and pulse velocity
formulae for a liquid whose viscosity varies with frequency // Physics in
Medicine andBiology. – 1959. – V. 2. P. 374–382.

66. Zhao R. Experimental and theoretical investigation of blood flow dynam-


ics associated with blood contacting devices: PhD Thesis / R. Zhao. –
Pittsburgh, 2008. – 176 p.

69

You might also like