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Old 02-14-2013, 12:14 PM   #46
MisterJoji
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Originally Posted by Circa89 View Post
J Biomech Eng. 2008 Feb;130(1):011003. doi: 10.1115/1.2838029.
Effect of blood viscosity on oxygen transport in residual stenosed artery following angioplasty.

Kwon O, Krishnamoorthy M, Cho YI, Sankovic JM, Banerjee RK.
Source

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

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 pO(2) decrease to shift radially outward by approximately 20% from the center of the artery for the basal flow, but by approximately 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 90 mm Hg 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 90 mm Hg for the basal flow. As Hct increases from 25% to 65%, the average of pO(2,min) beyond the diverging section drops by approximately 25% for the basal flow, whereas it increases by approximately 15% for the hyperemic flow. Thus, current results with the moderate stenosed artery indicate that reducing Hct might be favorable in terms of increasing O(2) flux and pO(2,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.
Did you read that before posting? That is a site specific study comparing coronary flows and it's effect with blood viscosity. People with coronary clots are regularly on blood thinners for 2 reasons, to prevent further clotting and to increase blood flow distal to the clot. Thinner blood has an easier time flowing past the clot because there is better laminar flow, thereby delivering more oxygen to the infarcting/injured area. The marginal increase in PO2 would have no effect on tissue oxygenation. Also PO2's run on different machines have an acceptable variance of +/- 6 so the slight increase in PO2 could just be from margin of error. Aside from fatigue from not being able to practice hard, blood thinners have pretty much no effect on oxygen content and delivery and would not cause a professional athlete any increased fatigue.
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