Cardiac and vascular disease prior to hatching in chick embryos incubated at high altitude

• Published in: Journal of developmental origins of health and disease 2010-02, Vol.1 (1), p.60-66
• Main Authors: Salinas, C. E., Blanco, C. E., Villena, M., Camm, E. J., Tuckett, J. D., Weerakkody, R. A., Kane, A. D., Shelley, A. M., Wooding, F. B. P., Quy, M., Giussani, D. A.
• Format: Article
• Language: English
• Subjects: Birth weight; Cardiovascular disease; Cardiovascular system; Coronary vessels; Eggs; Heart; Hypotheses; Hypoxia; Nutrition; Physiology; Pregnancy; Sea level
• ISSN: 2040-1744; 2040-1752
• DOI: 10.1017/S2040174409990043

The partial contributions of reductions in fetal nutrition and oxygenation to slow fetal growth and a developmental origin of cardiovascular disease remain unclear. By combining high altitude with the chick embryo model, we have previously isolated the direct effects of high-altitude hypoxia on growth. This study isolated the direct effects of high-altitude hypoxia on cardiovascular development. Fertilized eggs from sea-level or high-altitude hens were incubated at sea level or high altitude. Fertilized eggs from sea-level hens were also incubated at high altitude with oxygen supplementation. High altitude promoted embryonic growth restriction, cardiomegaly and aortic wall thickening, effects which could be prevented by incubating eggs from high-altitude hens at sea level or by incubating eggs from sea-level hens at high altitude with oxygen supplementation. Embryos from high-altitude hens showed reduced effects of altitude incubation on growth restriction but not on cardiovascular remodeling. The data show that: (1) high-altitude hypoxia promotes embryonic cardiac and vascular disease already evident prior to hatching and that this is associated with growth restriction; (2) the effects can be prevented by increased oxygenation; and (3) the effects are different in embryos from sea-level or high-altitude hens.