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Am J Physiol Heart Circ Physiol (May 20, 2004). doi:10.1152/ajpheart.00081.2004
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Submitted on February 2, 2004
Accepted on May 17, 2004

Measuring Hemodynamic Changes During Mammalian Development

E. A.V. Jones1, M. H. Baron2, S. E. Fraser3, and M. E. Dickinson3*

1 Department of Chemical Engineering, California Insitute of Technology, Pasadena, CA, USA
2 Molecular, Cellular and Developmental Biology, Mount Sinai School of Medicine, New York, NY, USA
3 Biology Imaging Center, California Insitute of Technology, Pasadena, CA, USA

* To whom correspondence should be addressed. E-mail: maryd{at}gg.caltech.edu.

The pathogenesis of many congenital cardiovascular diseases involves abnormal flow within the embryonic vasculature, resulting either from heart malformations or from defects in the vasculature itself. Extensive genetic and genomic analysis in the mouse has led to the identification of an array of mutations that result in cardiovascular defects during embryogenesis. Many of these mutations cause secondary effects within the vasculature which are thought to arise because of altered fluid dynamics. Presumably, cardiac defects disturb or reduce flow, leading to the disruption of the mechanical signals necessary for proper vascular development. Unfortunately, a precise understanding of how disruptions in flow lead to secondary defects in the vasculature has been hampered by the inadequacy of existing analytical tools. Here we use a fast line-scanning technique for the quantitative analysis of hemodynamics during early organogenesis in the mouse embryo and present a model system for studying cellular responses during the formation and remodeling of the mammalian cardiovascular system. Flow velocity profiles can be measured as soon as the heart begins to beat, even in newly formed vessels. These studies establish a link between the pattern of blood flow within the vasculature and the stage of heart development and enable the analysis of the influence of mechanical forces during development.




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