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. 2014 May 22;3(3):e000841. doi: 10.1161/JAHA.114.000841

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© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 8. — Effect of maternal O₂ deprivation on cardiac outlet morphogenesis. Pregnant mice were housed at 0.5 ATM (half of the normal O₂ content) from E10.5 to 13.5 and returned to normal conditions until E15.5. Sections shown are from E15.5 normoxic (A, C, E, and G) and hypoxic (B, D, F, and H) embryos from anterior to posterior with respect to the heart. B and D, The aorta of the hypoxic embryo is mal‐positioned originating partly from the RVOT in DORV morphology. More posteriorly is (F) VSD and (H) ASD with persistence of the AV cushion mesenchyme. Scale bars: 500 μm. Ao indicates aorta; ASD, atrial septal defect; ATM, atmospheres; DORV, double outlet right ventricle; LV, left ventricle; pa, pulmonary artery; RV, right ventricle; VSD, ventricular septal defect.