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Determination of Critical Parameters in Platelet Margination DANIEL A. REASOR JR., MARMAR MEHRABADI, DAVID N. KU, and CYRUS K. AIDUN George W. Woodruff School of Mechanical Engineering, and The Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, GA 30332, USA (Received 15 February 2012; accepted 23 August 2012; published online 11 September 2012) Associate Editor Konstantinos Konstantopoulos oversaw the review of this article.

requires a high rate of transport of platelets to the wall. The mechanism of platelet margination may guide us in identifying risk factors associated with atherothrombosis, and ways to prevent arterial occlusions. Since platelets are the predominant components of arterial thrombi,7,17 their transport rate to the thrombotic site plays an important role in the rate of thrombus growth. The presence of red blood cells (RBCs) in whole blood controls the rate of platelet flux to the vessel walls increasing it by several orders of magnitude compared to transport due to Brownian motion.61 This higher rate of transport and drift of platelets towards the vessels walls due to RBCs is termed enhanced diffusivity.27,51 Studies on thrombus growth employing continuum transport models, including phenomenological models of enhanced diffusivity, suggest that platelet transport may be a critical rate limiting process in thrombus growth at relevant pathophysiological shear rates.5,50 In addition to platelet concentration at the vicinity of vessel wall, platelets dynamics at this region may affect the rate of adhesion of platelets to the site of damage by changing collision frequency rate, collision contact time, and available surface area for contact.29,38 Due to the small time and length scales and optical properties of blood, the platelets dynamics near the vessel wall are not well understood. Platelets motions may be analogous to rolling motion of leukocytes on inflamed endothelium, but may exhibit more of a flipping motion due to its discoid shape. The bonds between platelet receptor glycoproteins GPIb and immobilized von Willebrand factor may be important in mediating and controlling this rolling motion.36 The flat shape of platelets, however, is unsuitable for rolling compared to the spherical shape of leukocytes. The study by Pozrikidis44 demonstrated that the rotation rate of a platelet-shaped particle undergoing flipping motions is exaggerated when adhesive forces and torques are not modeled. Experiments by Maxwell et al.35 have identified sliding as the most frequent mode of

Abstract—An investigation of margination dependence on hematocrit, platelet shape, and viscosity ratio of plasma to cytoplasm is presented. Whole blood is modeled as a suspension of deformable red blood cells (RBCs) and rigid platelets in a viscous liquid. The fluid phase is simulated using the lattice-Boltzmann method, the RBC membranes are modeled with a coarse-grained spectrin-link method, and the dynamics of rigid particles are updated using Newton’s equations of motion for axisymmetri