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Am J Physiol Heart Circ Physiol (May 19, 2006). doi:10.1152/ajpheart.00274.2006
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Submitted on March 16, 2006
Accepted on May 7, 2006

Allometric Scaling of Wall Shear Stress from Mouse to Man: Quantification Using Cine Phase-Contrast MRI and Computational Fluid Dynamics

Joan M Greve1, Andrea S Les1, Beverly T Tang2, Mary T Draney Blomme3, Nathan M Wilson3, Ronald L Dalman3, Norbert J Pelc4, and Charles Anthony Taylor5*

1 Bioengineering, Stanford University, Stanford, California, United States
2 Mechanical Engineering, Stanford University, Stanford, California, United States
3 Surgery, Stanford University, Stanford, California, United States
4 Bioengineering, Stanford University, Stanford, California, United States; Radiology, Stanford University, Stanford, California, United States
5 Bioengineering, Stanford University, Stanford, California, United States; Mechanical Engineering, Stanford University, Stanford, California, United States; Surgery, Stanford University, Stanford, California, United States

* To whom correspondence should be addressed. E-mail: taylorca{at}stanford.edu.

Allometric scaling laws relate structure or function between species of vastly different sizes. They have rarely been derived for hemodynamic parameters known to affect the cardiovascular system, e.g. wall shear stress (WSS). This work implemented non-invasive methods to quantify and determine a scaling law for WSS. Geometry and blood flow velocities in the infrarenal aorta of mice and rats under isoflurane anesthesia were quantified using 2D magnetic resonance angiography and phase-contrast MRI at 4.7T. Three dimensional models constructed from anatomical data were discretized and used for computational fluid dynamics simulations using phase contrast velocity imaging data as inlet boundary conditions. WSS was calculated along the infrarenal aorta and compared between species to formulate an allometric equation for WSS. Mean WSS along the infrarenal aorta was significantly greater in mice and rats compared to humans (87.6, 70.5, 4.8 dynes/cm2, p < 0.01) and a scaling exponent of -0.38 (R2 = 0.92) was determined. Manipulation of the murine genome has made small animal models standard surrogates for better understanding the healthy and diseased human cardiovascular system. It has therefore become increasingly important to understand how results scale from mouse to human. This non-invasive methodology provides the opportunity to serially quantify changes in WSS during disease progression and/or therapeutic intervention.




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