We present a 3D computational modeling study of the transport of micro-scale drug carriers modeled as microparticles of different shapes (spherical, oblate, and prolate) in whole blood represented as a suspension of deformable red blood cells. The objective is to quantify the effect of microparticle shapes on their margination, near-wall dynamics and adhesion. We observe that the near-wall accumulation is highest for oblate particles of moderate aspect ratio, followed by spherical particles, and lowest for very elongated prolate particles. The result is explained using micro-scale dynamics of individual particles, and their interaction with red blood cells. We observe that the orientation of microparticles in 3D space and the frequency of their collisions with red blood cells are the key factors affecting their margination. We show that due to repeated collisions with red blood cells in the presence of a bounding wall, the axes of revolution of oblate particles align near the plane of the shear flow, but those of prolate particles shift towards the vorticity axis with a wider distribution. Such specific orientations lead to more frequent collisions and a greater lateral drift for oblate particles than microspheres, but less frequent collisions and a reduced lateral drift for elongated prolate particles, resulting in the observed differences in their near-wall accumulation. Once marginated, the particle shape has an entirely different effect on the likelihood of making particle-wall contacts. We find that marginated prolate particles, due to their alignment along the vorticity axis and large angular fluctuations, are more likely to make contacts with the wall than spherical and oblate particles. We further simulate the adhesion between flowing microparticles and the wall in the presence of red blood cells, and observe that once wall contacts are established, the likelihood of firm adhesion is greater for disk-like particles, followed by elongated prolates, and microspheres. Consequently, this study suggests that the local hemorheological conditions near the targeted sites must be taken into consideration while selecting the optimum shape of micro-scale vascular drug carriers.
A high-fidelity computational model using a 3D immersed boundary method is used to study platelet dynamics in whole blood. We focus on the 3D effects of the platelet-red blood cell (RBC) interaction on platelet margination and near-wall dynamics in a shear flow. We find that the RBC distribution in whole blood becomes naturally anisotropic and creates local clusters and cavities. A platelet can enter a cavity and use it as an express lane for a fast margination toward the wall. Once near the wall, the 3D nature of the platelet-RBC interaction results in a significant platelet movement in the transverse (vorticity) direction and leads to anisotropic platelet diffusion within the RBC-depleted zone or cell-free layer (CFL). We find that the anisotropy in platelet motion further leads to the formation of platelet clusters, even in the absence of any platelet-platelet adhesion. The transverse motion, and the size and number of the platelet clusters are observed to increase with decreasing CFL thickness. The 3D nature of the platelet-RBC collision also induces fluctuations in off-shear plane orientation and, hence, a rotational diffusion of the platelets. Although most marginated platelets are observed to tumble just outside the RBC-rich zone, platelets further inside the CFL are observed to flow with an intermittent dynamics that alters between sliding and tumbling, as a result of the off-shear plane rotational diffusion, bringing them even closer to the wall. To our knowledge, these new findings are based on the fundamentally 3D nature of the platelet-RBC interaction, and they underscore the importance of using cellular-scale 3D models of whole blood to understand platelet margination and near-wall platelet dynamics.
The geometric confinement of TAV by the failed bioprosthesis or the calcified native valve increases the BRT on the TAV leaflets. This may act as a permissive factor in valve thrombosis.
A computational study is presented on the flow of deformable red blood cells in stenosed microvessels. It is observed that the Fahraeus-Lindqvist effect is significantly enhanced due to the presence of a stenosis. The apparent viscosity of blood is observed to increase by several folds when compared to non-stenosed vessels. An asymmetric distribution of the red blood cells, caused by geometric focusing in stenosed vessels, is observed to play a major role in the enhancement. The asymmetry in cell distribution also results in an asymmetry in average velocity and wall shear stress along the length of the stenosis. The discrete motion of the cells causes large time-dependent fluctuations in flow properties. The root-mean-square of flow rate fluctuations could be an order of magnitude higher than that in non-stenosed vessels. Several folds increase in Eulerian velocity fluctuation is also observed in the vicinity of the stenosis. Surprisingly, a transient flow reversal is observed upstream a stenosis but not downstream. The asymmetry and fluctuations in flow quantities and the flow reversal would not occur in absence of the cells. It is concluded that the flow physics and its physiological consequences are significantly different in micro- versus macrovascular stenosis.
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