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Cardiac and vascular disease prior to hatching in chick embryos incubated at high altitude
C E Salinas1, C E Blanco2, M Villena1
11Instituto Boliviano de Biología de Altura, Facultad de Medicina, Universidad Mayor de San Andrés, La Paz, Bolivia.
Insights
High altitude exposure causes embryonic growth restriction and cardiovascular disease in chick embryos. Increased oxygenation prevents these effects, highlighting the impact of hypoxia on fetal development.
Area of Science:
- Developmental Biology
- Cardiovascular Physiology
- Altitude Medicine
Background:
- Fetal nutrition and oxygenation are critical for healthy growth and cardiovascular development.
- The precise impact of reduced oxygen (hypoxia) on cardiovascular disease origins is not fully understood.
- Previous studies used high altitude and chick embryos to isolate hypoxia's effects on growth.
Purpose of the Study:
- To isolate and define the direct effects of high-altitude hypoxia on embryonic cardiovascular development.
- To investigate the association between hypoxia-induced growth restriction and cardiovascular changes.
- To compare the responses of embryos from sea-level and high-altitude hens to hypoxic conditions.
Main Methods:
- Incubation of fertilized eggs from sea-level or high-altitude hens under varying conditions: sea level, high altitude, and high altitude with oxygen supplementation.
- Utilized the chick embryo model to control for nutritional factors.
- Assessed embryonic growth, heart size (cardiomegaly), and aortic wall thickness.
Main Results:
- High altitude induced embryonic growth restriction, cardiomegaly, and aortic wall thickening.
- These effects were preventable by either returning high-altitude hen eggs to sea level or supplementing oxygen for sea-level hen eggs at high altitude.
- Embryos from high-altitude hens exhibited reduced growth restriction but not cardiovascular remodeling under altitude incubation.
- Hypoxia-induced cardiovascular and vascular disease is evident before hatching and linked to growth restriction.
Conclusions:
- High-altitude hypoxia directly promotes embryonic cardiac and vascular disease, associated with growth restriction.
- Adequate oxygenation can prevent these detrimental effects.
- Embryonic responses to high-altitude hypoxia differ between sea-level and high-altitude hen origins, suggesting potential adaptive mechanisms.
Abstract:
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.

