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Hyperoxia and local organ blood flow in the developing chick embryo
J M van Golde1, T A Mulder, E Scheve
1Department of Neonatology, University Hospital, Maastricht University, The Netherlands.vanGolde@voeding.tno.nl
The Journal of Physiology
|February 2, 1999
Summary
Developing chick embryos gain the ability to constrict blood vessels in response to high oxygen levels late in incubation. This protective mechanism, crucial for preventing hyperoxia toxicity, develops during the final 15% of the incubation period.
Area of Science:
- Physiology
- Developmental Biology
- Cardiovascular Research
Background:
- Hyperoxia, or high oxygen levels, can induce local vasoconstriction in adult organs as a protective response.
- The developmental timing of this vasoconstrictor capacity in embryonic development is not well understood.
Purpose of the Study:
- To investigate the onset of hyperoxia-induced vasoconstriction in developing chick embryos.
- To determine when during embryonic development the cardiovascular system develops protective mechanisms against hyperoxia.
Main Methods:
- Cardiac output (CO) distribution was measured in chick embryos across different incubation stages (10-19 days).
- Fluorescent microspheres were used to track blood flow distribution during normoxia and acute hyperoxia (100% O2) exposure (5 and 20 minutes).
- Organ-specific CO fractions were calculated based on microsphere fluorescence.
Main Results:
- Hyperoxia-induced vasoconstriction was observed only in late-stage embryos (18-19 days).
- In these late-stage embryos, CO decreased to the heart and carcass, while increasing to the yolk-sac and chorioallantoic membrane.
- A more pronounced response, including reduced CO to the brain, intestine, and liver, was seen after 20 minutes of hyperoxia.
Conclusions:
- Local mechanisms for hyperoxia-induced vasoconstriction develop late in chick embryo development.
- This critical protective response emerges during the final 15% of the 21-day incubation period.
- The findings highlight a critical developmental window for cardiovascular adaptation to high oxygen environments.