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Register a new userCluster of red blood cells in microcapillary flow: hydrodynamic versus macromolecule induced interaction
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Added by
Viviana Claver\\'ia
Publication date
2016
fields
Physics
and research's language is
English
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We present experiments on RBCs that flow through microcapillaries under physiological conditions. We show that the RBC clusters form as a subtle imbrication between hydrodynamics interaction and adhesion forces because of plasma proteins. Clusters form along the capillaries and macromolecule-induced adhesion contribute to their stability. However, at high yet physiological flow velocities, shear stresses overcome part of the adhesion forces, and cluster stabilization due to hydrodynamics becomes stronger. For the case of pure hydrodynamic interaction, cell-to-cell distances have a pronounced bimodal distribution. Our 2D-numerical simulations on vesicles captures the transition between adhesive and non-adhesive clusters at different flow velocities.
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Plasma proteins such as fibrinogen induce the aggregation of red blood cells (RBC) into rouleaux, which are responsible for the pronounced shear thinning behavior of blood, control the erythro- cyte sedimentation rate (ESR) a common hematological test and are involved in many situations of physiological relevance such as structuration of blood in the microcirculation or clot formation in pathological situations. Confocal microscopy is used to characterize the shape of RBCs within rouleaux at equilibrium as a function of macromolecular concentration, revealing the diversity of contact zone morphology. Three different configurations that have only been partly predicted before are identified, namely parachute, male-female and sigmoid shapes, and quantitatively recovered by numerical simulations. A detailed experimental and theoretical analysis of clusters of two cells shows that the deformation increases nonlinearly with the interaction energy. Models indicate a forward bifurcation in which the contacting membrane undergoes a buckling instability from a flat to a de- formed contact zone at a critical value of the interaction energy. These results are not only relevant for the understanding of the morphology and stability of RBC aggregates, but also for a whole class of interacting soft deformable objects such as vesicles, capsules or cells in tissues.
Using a multiscale blood flow solver, the complete diffusion tensor of nanoparticle (NP) in sheared cellular blood flow is calculated over a wide range of shear rate and haematocrit. In the short-time regime, NPs exhibit anomalous dispersive behaviors under high shear and high haematocrit due to the transient elongation and alignment of the red blood cells (RBCs). In the long-time regime, the NP diffusion tensor features high anisotropy. Particularly, there exists a critical shear rate ($sim$100 $s^{-1}$) around which the shear-rate dependence of the diffusivity tensor changes from linear to nonlinear scale. Above the critical shear rate, the cross-stream diffusivity terms vary sublinearly with shear rate, while the longitudinal term varies superlinearly. The dependence on haematocrit is linear in general except at high shear rates, where a sublinear scale is found for the vorticity term and a quadratic scale for the longitudinal term. Through analysis of the suspension microstructure and numerical experiments, the nonlinear hemorheological dependence of the NP diffusion tensor is attributed to the streamwise elongation and cross-stream contraction of RBCs under high shear, quantified by a Capillary number. The RBC size is shown to be the characteristic length scale affecting the RBC-enhanced shear-induced diffusion (RESID), while the NP size at submicron exhibits negligible influence on the RESID. Based on the observed scaling behaviors, empirical correlations are proposed to bridge the NP diffusion tensor to specific shear rate and haematocrit. The characterized NP diffusion tensor provides a constitutive relation that can lead to more effective continuum models to tackle large-scale NP biotransport applications.
We investigate the rheological characteristics of human blood plasma in shear and elongational flows. While we can confirm a Newtonian behavior in shear flow within experimental resolution, we find a viscoelastic behavior of blood plasma in the pure extensional flow of a capillary break-up rheometer. The influence of the viscoelasticity of blood plasma on capillary blood flow is tested in a microfluidic device with a contraction-expansion geometry. Differential pressure measurements revealed that the plasma has a pronounced flow resistance compared to that of pure water. Supplementary measurements indicate that the viscoelasticity of the plasma might even lead to viscoelastic instabilities under certain conditions. Our findings show that the viscoelastic properties of plasma should not be ignored in future studies on blood flow.
In the emerging field of 3D bioprinting, cell damage due to large deformations is considered a main cause for cell death and loss of functionality inside the printed construct. Those deformations, in turn, strongly depend on the mechano-elastic response of the cell to the hydrodynamic stresses experienced during printing. In this work, we present a numerical model to simulate the deformation of biological cells in arbitrary three-dimensional flows. We consider cells as an elastic continuum according to the hyperelastic Mooney-Rivlin model. We then employ force calculations on a tetrahedralized volume mesh. To calibrate our model, we perform a series of FluidFM(R) compression experiments with REF52 cells demonstrating that all three parameters of the Mooney-Rivlin model are required for a good description of the experimental data at very large deformations up to 80%. In addition, we validate the model by comparing to previous AFM experiments on bovine endothelial cells and artificial hydrogel particles. To investigate cell deformation in flow, we incorporate our model into Lattice Boltzmann simulations via an Immersed-Boundary algorithm. In linear shear flows, our model shows excellent agreement with analytical calculations and previous simulation data.
Driven or active suspensions can display fascinating collective behavior, where coherent motions or structures arise on a scale much larger than that of the constituent particles. Here, we report experiments and numerical simulations revealing that red blood cells (RBCs) assemble into regular patterns in a confined shear flow. The order is of pure hydrodynamic and inertialess origin, and emerges from a subtle interplay between (i) hydrodynamic repulsion by the bounding walls which drives deformable cells towards the channel mid-plane and (ii) intercellular hydrodynamic interactions which can be attractive or repulsive depending on cell-cell separation. Various crystal-like structures arise depending on RBC concentration and confinement. Hardened RBCs in experiments and rigid particles in simulations remain disordered under the same conditions where deformable RBCs form regular patterns, highlighting the intimate link between particle deformability and the emergence of order. The difference in structuring ability of healthy (deformable) and diseased (stiff) RBCs creates a flow signature potentially exploitable for diagnosis of blood pathologies.
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