Bulletin of the American Physical Society
68th Annual Meeting of the APS Division of Fluid Dynamics
Volume 60, Number 21
Sunday–Tuesday, November 22–24, 2015; Boston, Massachusetts
Session R23: Biofluids: Red Blood Cell Dynamics and Clotting |
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Chair: Xin Yong, State University of New York Room: 300 |
Tuesday, November 24, 2015 12:50PM - 1:03PM |
R23.00001: The flow of red blood cells in stenosed microvessels and the influence of red blood cells on wall-bounded rolling motion of microparticles Koohyar Vahidkhah, Peter Balogh, Prosenjit Bagchi In the first part of this work, we consider a 3D computational study of the flow of deformable red blood cells in stenosed microvessels. We observe that the apparent viscosity of blood increases by several folds, and the rate of increase with increasing vessel diameter is also higher than that in non-stenosed vessels, implying an enhancement of the well-known Fahraeus-Lindqvist effect. The flow of the red blood cells causes time-dependent fluctuations in the blood flow rate. The RMS of the flow rate oscillations in the stenosed vessel is observed to be significantly higher than that in the non-stenosed vessel. Furthermore, several folds increase in the Eulerian velocity fluctuations and a transient flow reversal upstream the stenosed region are also observed, which would not occur in absence of the cells. In the second part, we consider the adhesive rolling motion of wall-bounded microparticles in presence of flowing red blood cells in microvessels. We observe two contradictory role of the red blood cells: On one hand, the cells facilitate the establishment of the particle--wall contact, and, thereby, initiation of adhesion. On the other hand, they augment the rolling velocity of the particles. Implications of these results on the optimal design of drug carriers are discussed. [Preview Abstract] |
Tuesday, November 24, 2015 1:03PM - 1:16PM |
R23.00002: Reduced-order models of the coagulation cascade Kirk B. Hansen, Shawn C. Shadden Previous models of flow-mediated thrombogenesis have generally included the transport and reaction of dozens of biochemical species involved in the coagulation cascade.\footnote{K.\ Leiderman and A.L.\ Fogelson, Math Med Biol {\bf 28}(1), 47--84 (2010).} Researchers have shown, however, that thrombin generation curves can be accurately reproduced by a significantly smaller system of reactions.\footnote{R.\ Wagenvoord, P.W.\ Hemker, and H.C.\ Hemker, J Thromb Haemost {\bf 4}(6), 1331--1338 (2006).} These reduced-order models are based on the system of ordinary differential equations representative of a well-mixed system, however, not the system of advection-diffusion-reaction equations required to model the flow-mediated case. Additionally, they focus solely on reproducing the thrombin generation curve, although accurate representation of certain intermediate species may be required to model additional aspects of clot formation, e.g.\ interactions with activated and non-activated platelets. In this work, we develop a method to reduce the order of a coagulation model through optimization techniques. The results of this reduced-order model are then compared to those of the full system in several representative cardiovascular flows. [Preview Abstract] |
Tuesday, November 24, 2015 1:16PM - 1:29PM |
R23.00003: Mesoscopic Modeling of Blood Clotting: Coagulation Cascade and Platelets Adhesion Alireza Yazdani, Zhen Li, George Karniadakis The process of clot formation and growth at a site on a blood vessel wall involve a number of multi-scale simultaneous processes including: multiple chemical reactions in the coagulation cascade, species transport and flow. To model these processes we have incorporated advection-diffusion-reaction (ADR) of multiple species into an extended version of Dissipative Particle Dynamics (DPD) method which is considered as a coarse-grained Molecular Dynamics method. At the continuum level this is equivalent to the Navier-Stokes equation plus one advection-diffusion equation for each specie. The chemistry of clot formation is now understood to be determined by mechanisms involving reactions among many species in dilute solution, where reaction rate constants and species diffusion coefficients in plasma are known. The role of blood particulates, i.e. red cells and platelets, in the clotting process is studied by including them separately and together in the simulations. An agonist-induced platelet activation mechanism is presented, while platelets adhesive dynamics based on a stochastic bond formation/dissociation process is included in the model. [Preview Abstract] |
Tuesday, November 24, 2015 1:29PM - 1:42PM |
R23.00004: Effect of Strain Rate on the Deformation of Red Blood Cells Entering a Constriction Jordan Mancuso, William Ristenpart Although much work has investigated the stretching behavior of RBCs in shear flows, relatively little work has examined the deformation that occurs in the physiologically important extensional flow at the entrance to a constriction. In particular, there is currently no analytical model to predict the extent of deformation as a function of the strain rate in the constriction entrance. Here we experimentally elucidate the relationship between strain rate and the dynamic stretching behavior of RBCs as they enter a microfluidic constriction. We systematically varied the flow rate and the microchannel geometry to vary the strain rate, and we measured the resulting RBC deformations with high speed video. We demonstrate that the Kelvin Voigt model captures the stretching dynamics, and that the RBC membrane elastic shear modulus increases approximately linearly with increasing strain rate. [Preview Abstract] |
Tuesday, November 24, 2015 1:42PM - 1:55PM |
R23.00005: Chaotic dynamics of red blood cells in oscillating shear flow Prosenjit Bagchi, Daniel Cordasco A 3D computational study of deformable red blood cells in dilute suspension and subject to sinusoidally oscillating shear flow is considered. It is observed that the cell exhibits either a periodic motion or a chaotic motion. In the periodic motion, the cell reverses its orientation either about the flow direction or about the flow gradient, depending on the initial conditions. In certain parameter range, the initial conditions are forgotten and the cells become entrained in the same sequence of horizontal reversals. The chaotic dynamics is characterized by a nonperiodic sequence of horizontal and vertical reversals, and swings. The study provides the first conclusive evidence of the chaotic dynamics of fully deformable cells in oscillating flow using a deterministic numerical model without the introduction of any stochastic noise. An analysis of the chaotic dynamics shows that chaos is only possible in certain frequency bands when the cell membrane can rotate by a certain amount allowing the cells to swing near the maximum shear rate. We make a novel observation that the occurrence of the vertical or horizontal reversal depends only on whether a critical angle, that is independent of the flow frequency, is exceeded at the instant of flow reversal. [Preview Abstract] |
Tuesday, November 24, 2015 1:55PM - 2:08PM |
R23.00006: Mechanosensing Dynamics of Red blood Cells Jiandi Wan Mechanical stress-induced deformation of human red blood cells (RBCs) plays important physiopathological roles in oxygen delivery, blood rheology, transfusion, and malaria. Recent studies demonstrate that, in response to mechanical deformation, RBCs release adenosine-5'-triphosphate (ATP), suggesting the existence of mechanotransductive pathways in RBCs. Most importantly, the released ATP from RBCs regulates vascular tone and impaired release of ATP from RBCs has been linked to diseases such as type II diabetes and cystic fibrosis. To date, however, the mechanisms of mechanotransductive release of ATP from RBCs remain unclear. Given that RBCs experience shear stresses continuously during the circulation cycle and the released ATP plays a central role in vascular physiopathology, understanding the mechanotransductive release of ATP from RBCs will provide not only fundamental insights to the role of RBCs in vascular homeostasis but also novel therapeutic strategies for red cell dysfunction and vascular disease. This talk describes the main research in my group on integrating microfluidic-based approaches to study the mechanosensing dynamics of RBCs. Specifically, I will introduce a micro?uidic approach that can probe the dynamics of shear-induced ATP release from RBCs with millisecond resolution and provide quantitative understandings of the mechanosensitive ATP release processes in RBCs. Furthermore, I will also describe our recent findings about the roles of the Piezo1 channel, a newly discovered mechanosensitive cation channel in the mechanotransductive ATP release in RBCs. Last, possible functions of RBCs in the regulation of cerebral blood flow will be discussed. [Preview Abstract] |
Tuesday, November 24, 2015 2:08PM - 2:21PM |
R23.00007: Shape Recovery of Elastic Red Blood Cells from Shear Flow Induced Deformation in Three Dimensions Yan Peng, John Gounley Red blood cells undergo substantial shape changes in vivo. Modeled as an elastic capsule, the shape recovery of a three dimensional biconcave capsule from shear flow is studied for different preferred elastic and bending configuration. The fluid-structure interaction is modeled using the multiple-relaxation time lattice Boltzmann (LBM) and immersed boundary (IBM) methods. Based on the studies of the limited shape memory observed in three dimensions, the shape recovery is caused by the preferred elastic configuration, at least when paired with a constant spontaneous curvature. For these capsules, the incompleteness of the shape recovery observed precludes any conjecture about whether a single or multiple phase(s) are necessary to describe the recovery process. Longer simulations and a more stable methodology will be necessary. [Preview Abstract] |
Tuesday, November 24, 2015 2:21PM - 2:34PM |
R23.00008: A simple model to understand the role of membrane shear elasticity and stress-free shape on the motion of red blood cells in shear flow Annie Viallat, Manouk Abkarian, Jules Dupire The analytical model presented by Keller and Skalak on the dynamics of red blood cells in shear flow described the cell as a fluid ellipsoid of fixed shape. It was extended to introduce shear elasticity of the cell membrane. We further extend the model when the cell discoid physiological shape is not a stress-free shape. We show that spheroid stress-free shapes enables fitting experimental data with values of shear elasticity typical to that found with micropipettes and optical tweezers. For moderate shear rates (when RBCs keep their discoid shape) this model enables to quantitatively determine an effective cell viscosity, that combines membrane and hemoglobin viscosities and an effective shear modulus of the membrane that combines shear modulus and stress-free shape. This model allows determining RBC mechanical parameters both in the tanktreading regime for cells suspended in a high viscosity medium, and in the tumbling regime for cells suspended in a low viscosity medium. In this regime,a transition is predicted between a rigid-like tumbling motion and a fluid-like tumbling motion above a critical shear rate, which is directly related to the mechanical parameters of the cell. [Preview Abstract] |
Tuesday, November 24, 2015 2:34PM - 2:47PM |
R23.00009: Quantification of hydrodynamic factors influencing cell lateral migration Stephanie Nix, Yohsuke Imai, Takuji Ishikawa The study of the migration of blood cells perpendicular to the direction of blood flow, or lateral migration, is motivated by the differing behavior of the various types of blood cells. \textit{In vivo}, red blood cells are observed to flow in the central region of the blood vessel, particularly in the microcirculation, while other types of cells in the blood, including white blood cells and platelets, are observed to flow disproportionately near the vessel wall. However, the specifics regarding the effect of hydrodynamic and biological factors are still unknown. Thus, in this study, we aim to quantify the effect of hydrodynamic factors on a cell model numerically using the boundary integral method. By using the boundary integral method, we can isolate the effect of a single hydrodynamic factor, such as a wall or given flow distribution, in an otherwise infinite flow. Then, we can use the obtained numerical results to develop a semi-analytical model describing the cell lateral migration dependent on only the flow geometry and the viscosity ratio between the cell and external fluid. [Preview Abstract] |
Tuesday, November 24, 2015 2:47PM - 3:00PM |
R23.00010: Coarse-grained theory to predict red blood cell migration in pressure-driven flow at zero Reynolds number Qin M. Qi, Vivek Narsimhan, Eric S.G. Shaqfeh The pressure-driven flow of blood in a rectangular channel is studied via the development of a modified Boltzmann collision theory. It is well known that the deformability of red blood cells(RBC) creates a hydrodynamic lift away from the channel walls and most importantly, forms a cell-free or “Fahraeus-Lindqvist” layer at the wall. A theory is presented to predict the uneven concentration distribution of RBCs in the cross-stream direction. We demonstrate that cell migration is mainly due to the balance between the hydrodynamic lift from the wall and cell-cell binary collisions. Each of these components is determined independently via boundary element simulations. The lift velocity shows a scaling with wall displacement law similar to that from previous vesicle experiments. The collisional displacements vary nonlinearly with cross-stream positions –a key input to the theory. Unlike the case of simple shear flow, a nonlocal shear rate correction is necessary to overcome the problem of zero lift and collision at the centerline. Finally a diffusional term is added to account for higher order collisions. The results indicate a decrease in cell-free layer thickness with increasing RBC volume fraction that is in good agreement with simulation of blood in 10-20\% range of hematocrit. [Preview Abstract] |
Tuesday, November 24, 2015 3:00PM - 3:13PM |
R23.00011: Experimental comparison of mammalian and avian blood flow in microchannels Kathryn Fink, Dorian Liepmann The non-Newtonian, shear rate dependent behavior of blood in microchannel fluid dynamics has been studied for nearly a century, with a significant focus on the characteristics of human blood. However, for over 200 years biologists have noted significant differences in red blood cell characteristics across vertebrate species, with particularly drastic differences in cell size and shape between mammals and non-mammalian classes. We present an experimental analysis of flow in long microchannels for several varieties of mammalian and avian blood, across a range of hematocrits, channel diameters, and flow rates. Correlation of shear rate and viscosity is compared to existing constitutive equations for human blood to further quantify the importance of red blood cell characteristics. Ongoing experimental results are made available in an online database for reference or collaboration. [Preview Abstract] |
Tuesday, November 24, 2015 3:13PM - 3:26PM |
R23.00012: Patient-specific modeling and analysis of dynamic behavior of individual sickle red blood cells under hypoxic conditions Xuejin Li, E. Du, Zhen Li, Yu-Hang Tang, Lu Lu, Ming Dao, George Karniadakis Sickle cell anemia is an inherited blood disorder exhibiting heterogeneous morphology and abnormal dynamics under hypoxic conditions. We developed a {\em time-dependent} cell model that is able to simulate the dynamic processes of repeated sickling and unsickling of red blood cells (RBCs) under physiological conditions. By using the kinetic cell model with parameters derived from {\em patient-specific} data, we present a mesoscopic computational study of the dynamic behavior of individual sickle RBCs flowing in a microfluidic channel with multiple microgates. We investigate how individual sickle RBCs behave differently from healthy ones in channel flow, and analyze the alteration of cellular behavior and response to single-cell capillary obstruction induced by cell rheologic rigidification and morphological change due to cell sickling under hypoxic conditions. We also simulate the flow dynamics of sickle RBCs treated with hydroxyurea (HU) and quantify the relative enhancement of hemodynamic performance of HU. [Preview Abstract] |
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