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Prenatal hyperoxia blunts the hypoxic ventilatory chemosensitivity of the 1-day old chicken hatchling
1Department of Physiology, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec H3G 1Y6, Canada.
Insights
Prenatal hyperoxia exposure in chickens significantly blunts the ventilatory response to hypoxia in newborns. This suggests prenatal oxygen levels impact respiratory development and carotid body function.
Area of Science:
- Physiology
- Developmental Biology
- Respiratory Medicine
Background:
- Prenatal hypoxia is known to impair the newborn's ventilatory response to hypoxia.
- This impairment is thought to stem from developmental disturbances in peripheral chemoreceptors.
- The effect of prenatal hyperoxia on chemoreceptor development and function remains less understood.
Purpose of the Study:
- To investigate the impact of prolonged prenatal hyperoxia on the ventilatory (V˙(E)) response to hypoxia in newborn chickens.
- To determine if prenatal hyperoxia affects respiratory responses to hypercapnia.
- To explore the potential role of carotid body dysfunction in observed respiratory changes.
Main Methods:
- Chicken hatchlings were exposed to 40% or 60% O2 during the final week of incubation and hatching.
- Ventilatory patterns and responses to hypoxia (10% and 15% O2) and hypercapnia were measured using a modified barometric technique.
- Control groups were incubated under normoxic conditions.
Main Results:
- Prenatal hyperoxia significantly reduced the V˙(E) response to 10% O2 by over 50% compared to controls.
- Hypoxic oxygen consumption (V˙(O2)) drop was more pronounced in hyperoxia-exposed hatchlings.
- The V˙(E) response to hypercapnia was largely unaffected, indicating no significant mechanical limitations to breathing.
Conclusions:
- Sustained prenatal hyperoxia, similar to prenatal hypoxia, impairs the newborn's ventilatory response to hypoxia.
- These findings suggest that altered prenatal oxygenation impacts carotid body function.
- The study supports the view that prenatal oxygen exposure is critical for normal chemoreceptor development and respiratory control.
Abstract:
Hypoxia sustained during the prenatal period lowers the ventilatory (V˙(E)) response to hypoxia of the newborn. This phenomenon probably results from a disturbance in the normal development of the peripheral chemoreceptors, as shown to be the case postnatally after sustained period of low or high oxygen. To test the possibility that prolonged prenatal hyperoxia may have a similar effect, the breathing pattern and the V˙(E) responses to hypoxia or hypercapnia were measured by a modification of the barometric technique in 1-day old chicken hatchlings exposed to 40% O2 or 60% O2 (N=16 each) during the last week of incubation (hatching included), and in controls incubated in normoxia (N=16). During air breathing and moderate hypoxia (15% O2), neither group differed from controls. However, the V˙(E) response to 10% O2 was reduced to less than half normal in both groups of prenatal-hyperoxia hatchlings. The hypoxic drop in oxygen consumption V˙(O2) was more marked than in controls, which probably helped to limit the degree of hypoxemia and to sustain the hyperventilation (increase in V˙(E)-V˙(O2) ratio). The V˙(E) response to hypercapnia was almost normal, suggesting that there was no mechanical limitation on V˙(E). The degree of blunting in the V˙(E) response to hypoxia was very similar to that previously measured in hatchlings exposed to hypoxia during the last week of incubation. The results support to the view that sustained changes in oxygenation during the prenatal period reduce the newborn's V˙(E) response to hypoxia probably because of a major dysfunction of the carotid bodies.
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