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Research Papers

# Effect of Blood Viscosity on Oxygen Transport in Residual Stenosed Artery Following Angioplasty

[+] Author and Article Information
Ohwon Kwon, Mahesh Krishnamoorthy

Department of Mechanical Engineering, University of Cincinnati, Cincinnati, OH 45221

Young I. Cho

Department of Mechanical Engineering and Mechanics, Drexel University, Philadelphia, PA 19104

John M. Sankovic

Microgravity Science Division, NASA Glenn Research Center, Cleveland, OH 44135

Rupak K. Banerjee1

Department of Mechanical Engineering, University of Cincinnati, Cincinnati, OH 45221; Department of Biomedical Engineering, University of Cincinnati, Cincinnati, OH 45221rupak.banerjee@uc.edu

1

Corresponding author. Also at Department of Mechanical, Industrial, and Nuclear Engineering, 688 Rhodes Hall, P.O. Box 210072, University of Cincinnati, OH 45221-0072.

J Biomech Eng 130(1), 011003 (Feb 05, 2008) (11 pages) doi:10.1115/1.2838029 History: Received July 17, 2006; Revised June 12, 2007; Published February 05, 2008

## Abstract

The effect of blood viscosity on oxygen transport in a stenosed coronary artery during the postangioplasty scenario is studied. In addition to incorporating varying blood viscosity using different hematocrit (Hct) concentrations, oxygen consumption by the avascular wall and its supply from vasa vasorum, nonlinear oxygen binding capacity of the hemoglobin, and basal to hyperemic flow rate changes are included in the calculation of oxygen transport in both the lumen and the avascular wall. The results of this study show that oxygen transport in the postangioplasty residual stenosed artery is affected by non-Newtonian shear-thinning property of the blood viscosity having variable Hct concentration. As Hct increases from 25% to 65%, the diminished recirculation zone for the increased Hct causes the commencement of $pO2$ decrease to shift radially outward by $∼20%$ from the center of the artery for the basal flow, but by $∼10%$ for the hyperemic flow at the end of the diverging section. Oxygen concentration increases from a minimum value at the core of the recirculation zone to over $90mmHg$ before the lumen-wall interface at the diverging section for the hyperemic flow, which is attributed to increased shear rate and thinner lumen boundary layer for the hyperemic flow, and below $90mmHg$ for the basal flow. As Hct increases from 25% to 65%, the average of $pO2,min$ beyond the diverging section drops by $∼25%$ for the basal flow, whereas it increases by $∼15%$ for the hyperemic flow. Thus, current results with the moderate stenosed artery indicate that reducing Hct might be favorable in terms of increasing $O2$ flux and $pO2,min$, in the medial region of the wall for the basal flow, while higher Hct is advantageous for the hyperemic flow beyond the diverging section. The results of this study not only provide significant details of oxygen transport under varying pathophysiologic blood conditions such as unusually high blood viscosity and flow rate, but might also be extended to offer implications for drug therapy related to blood-thinning medication and for blood transfusion and hemorrhage.

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## Figures

Figure 1

Geometry of a moderately stenosed artery (64% area occlusion)

Figure 2

Viscosity curves with Hct variations from 25% to 65%

Figure 3

Oxygen concentration contours (δ=300μm) for the basal flow (a) and the hyperemic flow (b)

Figure 4

Radial pO2 variation in the recirculation region (δ=300μm) for the basal flow (a) and the hyperemic flow (b)

Figure 5

Effect of Hct variations on the pO2,wall along the axial length (δ=300μm) for the basal flow (a) and the hyperemic flow (b)

Figure 6

Effect of Hct variations on oxygen flux and shear stress at the lumen-wall interface (Q=50ml∕min, δ=300μm)

Figure 7

Comparison of oxygen flux between basal and hyperemic flows

Figure 8

Variation of pO2,min at the wall along the axial length (δ=300μm) for the basal flow (a) and the hyperemic (b)

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