Altered Wall Shear Stresses in Embryonic Chicken Outflow Tract Due to Homocysteine Exposure

The embryonic heart is already beating before cardiac morphogenesis is complete. Therefore, the effect of blood flow on cardiogenesis has been subject of many studies. Shear stress, acting on the endocardial cells, has been shown to alter the expression of shear-responsive genes implicated in heart development. The congenital heart defects (CHDs) induced in the chicken embryo after altering blood flow and intracardiac shear stress are comparable to the type of defects observed after homocysteine (Hcy) exposure. This may suggest that altered blood flow and shear stress have a role in the etiology of Hcy-induced CHDs. The aim of this study is to quantitate wall shear stress (WSS) in the outflow tract (OFT) of Hcy-exposed chicken embryos. WSS was derived from the velocity field obtained with microscopic particle image velocimetry in the OFT of the embryonic-day-3 Hcy- and sham-treated chicken embryos. Hcy treatment consisted of L-Hcy-thiolactone 30 mu M solution injected into the neural tube of the embryos. The results suggest that Hcy has an inhibiting effect on WSS in the early embryonic chicken heart. These alterations in shear stress may cause altered gene expression and behaviour of endothelial cells, eventually contributing to the development of CHDs.