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Impact of hypoxia on early chick embryo growth and cardiovascular function
Sumeet K Sharma1, Jennifer L Lucitti, Cory Nordman
1Department of Pediatrics, Children's Hospital of Pittsburgh, Pennsylvania 15213, USA.
Insights
Early embryonic exposure to low oxygen (hypoxia) impairs cardiovascular development and function. This study shows hypoxia reduces embryo survival, growth, and cardiac performance, highlighting oxygen
Area of Science:
- Developmental biology
- Cardiovascular physiology
- Embryology
Background:
- Oxygen tension is crucial for embryonic and fetal development.
- While mature hearts are sensitive to hypoxia, the immature myocardium's response is less understood.
- Chronic hypoxia affects cardiovascular function in late fetuses and newborns.
Purpose of the Study:
- To investigate the impact of hypoxia during early cardiovascular (CV) morphogenesis on embryonic CV function and growth.
- To test if immature embryonic hearts are sensitive to hypoxia during critical developmental periods.
Main Methods:
- Fertile white Leghorn chick embryos were incubated in 15% oxygen (hypoxia) or 21% oxygen (control) until Hamburger-Hamilton stage 21 (3.5 days).
- In ovo viability, dysmorphic features, ventricular pressure and dimensions, and dorsal aortic arterial impedance were assessed.
- Key cardiovascular parameters including heart rate, ventricular pressures, volumes, ejection fraction, and arterial afterload were measured.
Main Results:
- Chronic hypoxia significantly decreased embryo viability and wet weight.
- Hypoxia impaired embryonic systolic function, evidenced by decreased maximum ventricular +dP/dt, peak pressure, and ejection fraction, alongside increased end-systolic volume.
- Arterial afterload (peripheral resistance) increased, while dorsal aortic stroke volume and hydraulic power decreased under hypoxic conditions.
Conclusions:
- Reduced oxygen tension during early cardiac development depresses ventricular function and increases cardiac afterload.
- Hypoxia delays embryonic growth and decreases embryo survival rates.
- A critical threshold of oxygen tension is necessary to support early embryonic morphogenesis and cardiovascular function.
Abstract:
Oxygen tension is a critical factor for appropriate embryonic and fetal development. Chronic hypoxia exposure alters cardiovascular (CV) function and structure in the late fetus and newborn, yet the immature myocardium is considered to be less sensitive to hypoxia than the mature heart. We tested the hypothesis that hypoxia during the period of primary CV morphogenesis impairs immature embryonic CV function and embryo growth. We incubated fertile white Leghorn chick embryos in 15% oxygen (hypoxia) or 21% oxygen (control) until Hamburger-Hamilton stage 21 (3.5 d). We assessed in ovo viability and dysmorphic features and then measured ventricular pressure and dimensions and dorsal aortic arterial impedance at stage 21. Chronic hypoxia decreased viability and embryonic wet weight. Chronic hypoxia did not alter heart rate or the ventricular diastolic indices of end-diastolic pressure, maximum ventricular -dP/dt, or tau. Chronic hypoxia decreased maximum ventricular +dP/dt and peak pressure, increased ventricular end-systolic volume, and decreased ventricular ejection fraction, consistent with depressed systolic function. Arterial afterload (peripheral resistance) increased and both dorsal aortic SV and steady-state hydraulic power decreased in response to hypoxia. Thus, reduced oxygen tension during early cardiac development depresses ventricular function, increases ventricular impedance (afterload), delays growth, and decreases embryo survival, suggesting that a critical threshold of oxygen tension is required to support morphogenesis and cardiovascular function in the early embryo.
