Hemodynamics in the mouse aortic arch as assessed by MRI, ultrasound, and numerical modeling

1 Mouse Imaging Centre, Hospital for Sick Children, Toronto; 2 Department of Medical Biophysics, University of Toronto; 3 Department of Mathematics, Mahidol University, Bangkok, Thailand; 4 Department of Mechanical and Industrial Engineering, University of Toronto; 5 St. Michael's Hospital, Tor...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2007-02, Vol.292 (2), p.H884-H892
Hauptverfasser: Feintuch, Akiva, Ruengsakulrach, Permyos, Lin, Amy, Zhang, Ji, Zhou, Yu-Qing, Bishop, Jonathon, Davidson, Lorinda, Courtman, David, Foster, F. Stuart, Steinman, David A, Henkelman, R. Mark, Ethier, C. Ross
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Sprache:eng
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Zusammenfassung:1 Mouse Imaging Centre, Hospital for Sick Children, Toronto; 2 Department of Medical Biophysics, University of Toronto; 3 Department of Mathematics, Mahidol University, Bangkok, Thailand; 4 Department of Mechanical and Industrial Engineering, University of Toronto; 5 St. Michael's Hospital, Toronto; 6 Sunnybrook Health Sciences Centre, Toronto; and 7 Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada Submitted 25 July 2006 ; accepted in final form 20 September 2006 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 modeling 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. atherogenesis; magnetic resonance imaging; finite element modeling; shear stress Address for reprint requests and other correspondence: C. R. Ethier, Institute of Biomaterials and Biomedical Engineering, Univ. of Toronto, 164 College St., Toronto, ON M5S 3G9 Canada (e-mail: ethier{at}mie.utoronto.ca )
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00796.2006