Interactions of blood cell constituents: Experimental investigation and computational modeling by discrete particle dynamics algorithm (original) (raw)
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Journal of Colloid and Interface Science, 2003
We investigate the physical mechanism of aggregation of red blood cells (RBC) in capillary vessels, using a discrete particle model. This model can accurately capture the scales from 0.001µm to 100µm, far below the scales, which can be modeled numerically with classical computational fluid dynamics. We use a discrete-particle model in 3D for modeling the flow of plasma and RBCs in a capillary tube. The two situations involving necking and no necking have been considered. The flexible viscoelastic red blood cells and the walls of the elastic vessel are made up of solid particles held together by elastic harmonic forces. The blood plasma is represented by a system of dissipative fluid particles. We have simulated the flow of cells of different shapes, such as normal and "sickle" cells. The cells coagulate in spite of the absence of adhesive forces in the model. The total number of fluid and solid particles used ranges from 1 to 3 million. We conclude that aggregation of red blood cells in capillary vessels is stimulated by depletion forces and hydrodynamic interactions. The cluster of "sickle" cells formed in the necking of the conduit efficiently decelerates the flow, while normal cells can pass through. These qualitative results from numerical simulations accord well with laboratory findings.
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Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences, 2008
Aim . Arterial occlusion is a leading cause of cardiovascular disease. The main mechanism causing vessel occlusion is thrombus formation, which may be initiated by the activation of platelets. The focus of this study is on the mechanical aspects of platelet-mediated thrombosis which includes the motion, collision, adhesion and aggregation of activated platelets in the blood. A review of the existing continuum-based models is given. A mechanical model of platelet accumulation onto the vessel wall is developed using the dissipative particle dynamics (DPD) method in which the blood (i.e. colloidal-composed medium) is treated as a group of mesoscale particles interacting through conservative, dissipative, attractive and random forces. Methods . Colloidal fluid components (plasma and platelets) are discretized by mesoscopic (micrometre-size) particles that move according to Newton's law. The size of each mesoscopic particle is small enough to allow tracking of each constituent of the...
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Annals of Biomedical Engineering, 2008
Platelet activation, adhesion, and aggregation on the blood vessel and implants result in the formation of mural thrombi. Platelet dynamics in blood flow is influenced by the far more numerous erythrocytes (RBCs). This is particularly the case in the smaller blood vessels (arterioles) and in constricted regions of blood flow (such as in valve leakage and hinge regions) where the dimensions of formed elements of blood become comparable with that of the flow geometry. In such regions, models to predict platelet motion, activation, aggregation and adhesion must account for platelet-RBC interactions. This paper studies platelet-RBC interactions in shear flows by performing simulations of micro-scale dynamics using a computational fluid dynamics (CFD) model. A level-set sharp-interface immersed boundary method is employed in the computations in which RBC and platelet boundaries are tracked on a two-dimensional Cartesian grid. The RBCs are assumed to have an elliptical shape and to deform elastically under fluid forces while the platelets are assumed to behave as rigid particles of circular shape. Forces and torques between colliding blood cells are modeled using an extension of the soft-sphere model for elliptical particles. RBCs and platelets are transported under the forces and torques induced by fluid flow and cell-cell and cell-platelet collisions. The simulations show that platelet migration toward the wall is enhanced with increasing hematocrit, in agreement with past experimental observations. This margination is seen to occur due to hydrodynamic forces rather than collisional forces or volumetric exclusion effects. The effect of fluid shear forces on the platelets increases exponentially as a function of hematocrit for the range of parameters covered in this study. The micro-scale analysis can be potentially employed to obtain a deterministic relationship between fluid forces and platelet activation and aggregation in blood flow past cardiovascular implants.
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Computational simulations using a two-dimensional lattice-Boltzmann immersed boundary method were conducted to investigate the motion of platelets near a vessel wall and close to an intravascular thrombus. Physiological volume fractions of deformable red blood cells and rigid platelet-size elliptic particles were studied under arteriolar flow conditions. Tumbling of platelets in the red-blood-cell depleted zone near the vessel walls was strongly influenced by nearby red blood cells. The thickness of the red-blood-cell depleted zone was greatly reduced near a thrombus, and platelets in this zone were pushed close to the surface of the thrombus to distances that would facilitate their cohesion to it. The distance, nature, and duration of close platelet-thrombus encounters were influenced by the porosity of the thrombus. The strong influence on platelet-thrombus encounters of red-blood-cell motion and thrombus porosity must be taken into account to understand the dynamics of platelet attachment to a growing thrombus.
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International Journal for Numerical Methods in Biomedical Engineering, 2010
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Mathematical Modelling of Natural Phenomena, 2014
Properties of blood cells and their interaction determine their distribution in flow. It is observed experimentally that erythrocytes migrate to the flow axis, platelets to the vessel wall, and leucocytes roll along the vessel wall. In this work, a three-dimensional model based on Dissipative Particle Dynamics method and a new hybrid (discrete-continuous) model for blood cells is used to study the interaction of erythrocytes with platelets and leucocytes in flow. Erythrocytes are modelled as elastic highly deformable membranes, while platelets and leucocytes as elastic membranes with their shape close to a sphere. Separation of erythrocytes and platelets in flow is shown for different values of hematocrit. Erythrocyte and platelet distributions are in a good qualitative agreement with the existing experimental results. Migration of leucocyte to the vessel wall and its rolling along the wall is observed.
A particle dynamic model of red blood cell aggregation kinetics
Annals of biomedical …, 2009
To elucidate the relationship between microscopic red blood cell (RBC) interactions and macroscopic rheological behavior, we propose a two-dimensional particle model capable of mimicking the main characteristics of RBC aggregation kinetics. The mechanical model of RBCs sheared in Couette flow is based on Newton law. We assumed a hydrodynamic force to move particles, a force to describe aggregation and an elasticity force. The role of molecular mass and concentration of neutral polymers on aggregation [Neu, B., and H. J. Meiselman. Biophys. J. 83:2482-2490] could be mimicked. Specifically, it was shown that for any shear rate (SR), the mean aggregate size (MAS) grew with time until it reached a constant value, which is consistent with in vitro experiments. It was also demonstrated that we could mimic the modal relationship between MAS and SR and the occurrence of maximum aggregation at about 0.1 s À1 . As anticipated, simulations indicated that an increase in aggregation force augmented MAS. Further, augmentation of the depletion layer thickness influenced MAS only for SR close to zero, which is a new finding. To conclude, our contribution reveals that the aggregation force intensity and SR influence the steady state MAS, and that the depletion and layer thickness affect the aggregation speed.
Modelling of thrombus growth and growth stop in flow by the method of dissipative particle dynamics
Russian Journal of Numerical Analysis and Mathematical Modelling, 2012
Platelet aggregation at the site of vascular injury leads to formation of a hemostatic plug covering the injury site, or a thrombus in the pathological case. The mechanisms that control clot growth and which lead to growth arrest are not yet completely understood. In order to study these mechanisms theoretically, we use the Dissipative Particle Dynamics method which allows us to model individual platelets in the flow and in the clot. The model takes into account different stages of platelet adhesion process. First, a platelet is captured reversibly by the aggregate, and then it activates and adheres firmly becoming a part of its core. We suggest that the core of the clot is composed of platelets unable to attach new platelets from the flow due to activation by thrombin and/or wrapping by the fibrin mesh. The simulations are in a good agreement with the experimental results . Modelling shows that stopping of growth of a hemostatic plug (and thrombus) can result from removing its exterior part by flow and exposing its non-adhesive core to the flow.