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Analysis of mechanisms for platelet near-wall excess under arterial blood flow conditions

Published online by Cambridge University Press:  11 April 2011

L. CROWL*
Affiliation:
Department of Mathematics, University of Utah, 155 South 1400 East, Salt Lake City, UT 84112, USA
A. L. FOGELSON
Affiliation:
Department of Mathematics and Department of Bioengineering, 155 South 1400 East, University of Utah, Salt Lake City, UT 84112, USA
*
Email address for correspondence: [email protected]

Abstract

The concentration of platelets near the blood vessel wall is important because platelets survey the condition of the vessel wall and respond to injuries to it. Under arterial flow conditions, platelets are non-uniformly distributed across the vessel lumen and have a high concentration within a few microns of the vessel wall. This is believed to be a consequence of the complex motion of red blood cells which constitute a large fraction of the blood's volume. We use a novel lattice Boltzmann-immersed boundary method to simulate, in two dimensions, the motion of dense red blood cell suspensions and their effect on platelet-sized particles. We track the development of a red blood cell-free layer near the wall and the later development of the platelet near-wall excess. We find that the latter develops more quickly at high wall shear rates and that the magnitude of the excess and its proximity to the wall are dependent on haematocrit. Treating the simulation data as if it were generated by a drift–diffusion process, we find that the effective lateral platelet diffusivity depends strongly on lateral position; it has a magnitude of order of 10−6 cm2 s−1 over much of the lumen but drops to almost zero close to the wall. This large effective diffusivity over the core of the lumen combined with reduced space for platelets in this region because of the inward migration of red blood cells largely but not completely accounts for the observed platelet-concentration profiles. We present evidence for a highly localized red blood cell-induced platelet drift at the edge of the red cell-free layer and suggest a physical mechanism that may generate it.

Type
Papers
Copyright
Copyright © Cambridge University Press 2011

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