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Am J Physiol Heart Circ Physiol (September 29, 2006). doi:10.1152/ajpheart.00796.2006
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Submitted on July 25, 2006
Accepted on September 20, 2006

Hemodynamics in the Mouse Aortic Arch as Assessed by MRI, Ultrasound and Numerical Modeling

Akiva Feintuch1, Permyos Ruengsakulrach2, Amy Lin3, Ji Zhang3, Yuqing Zhou1, Jonathon Bishop1, Lorinda Davidson1, David Courtman4, F. Stuart Foster5, David Steinman6, R. Mark Henkelman7, and C. Ross Ethier6*

1 Mouse Imaging Centre, Hospital for Sick Children, Toronto, Canada
2 Department of Mathematics, Mahidol University, Bangkok, Thailand
3 Department of Mechanical & Industrial Engineering, University of Toronto, Toronto, Canada
4 St. Michael's Hospital, Toronto, Canada
5 Sunnybrook Health Sciences Centre, Toronto, Canada
6 Department of Mechanical & Industrial Engineering, University of Toronto, Toronto, Canada; Institute for Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Canada
7 Mouse Imaging Centre, Hospital for Sick Children, Toronto, Canada; Department of Medical Biophysics, University of Toronto, Toronto, Canada

* To whom correspondence should be addressed. E-mail: ethier{at}mie.utoronto.ca.

Mice are widely used to study arterial disease in humans, and the pathogenesis of arterial diseases is known to be strongly influenced by hemodynamic factors. It is therefore of interest to characterize the hemodynamic environment in the mouse arterial tree. Previous measurements have suggested that many relevant hemodynamic variables are similar between the mouse and the human. Here we use a combination of Doppler ultrasound and MRI measurements, coupled with numerical modelling techniques, to characterize the hemodynamic environment in the mouse aortic arch at high spatial resolution. We find that the hemodynamically-induced stresses on arterial endothelial cells are much larger in magnitude and more spatially uniform in the mouse than in the human, an effect that can be explained by fluid mechanical scaling principles. This surprising finding seems to be at variance with currently accepted models of the role of hemodynamics in atherogenesis and the known distribution of atheromatous lesions in mice.




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