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Ventilatory response to hypoxia in chicken hatchlings: a developmental window of sensitivity to embryonic hypoxia
Kirsten Ferner1, Jacopo P Mortola
1Department of Physiology, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec, H3G 1Y6 Canada. kirsten.ferner@museum.hu-berlin.de
Insights
Prenatal hypoxia exposure during the final week of incubation impairs ventilatory chemosensitivity in chicken hatchlings. This suggests the last days of embryonic development are critical for developing normal respiratory responses to oxygen and carbon dioxide levels.
Area of Science:
- Physiology
- Developmental Biology
- Respiratory Medicine
Background:
- Previous research indicated embryonic hypoxia blunts ventilatory chemosensitivity in hatchlings.
- Carotid bodies, crucial for respiratory control, mature during the late stages of embryonic development.
Purpose of the Study:
- To determine if the final week of incubation is a critical period for hypoxia-induced effects on ventilatory chemosensitivity.
- To investigate the impact of hypoxia during specific incubation periods on hatchling respiratory responses.
Main Methods:
- Chicken eggs were exposed to normoxia (21% O2) or hypoxia (15% O2) throughout incubation (HxTot) or during the 1st (Hx1), 2nd (Hx2), or 3rd week (Hx3).
- Pulmonary ventilation and oxygen consumption were measured in hatchlings.
- Ventilatory chemosensitivity was assessed by exposing hatchlings to acute hypoxia and hypercapnia.
Main Results:
- Hypoxia during the entire incubation (HxTot) and the final week (Hx3) significantly decreased responses to acute hypoxia compared to controls.
- Responses to acute hypercapnia were blunted only in the HxTot group.
- No significant differences in body weight or hatching time (except HxTot) were observed across groups.
Conclusions:
- The third week of embryonic development is a critical period for the impact of hypoxia on ventilatory chemosensitivity to hypoxia.
- Prenatal hypoxia appears to impair ventilatory chemosensitivity by interfering with carotid body development.
- These findings highlight the sensitivity of late-term embryonic development to hypoxic conditions.
Abstract:
We had reported previously [Szdzuy, K., Mortola, J.P., 2007b. Ventilatory chemosensitivity of the 1-day-old chicken hatchling after embryonic hypoxia. Am. J. Physiol. (Regul. Integr. Comp. Physiol.) 293, R1640-R1649] that hypoxia during incubation blunted ventilatory chemosensitivity in the hatchling. Because the carotid bodies become functional in the last portion of incubation, we asked whether these last days were the critical period for the effects of hypoxia on the development of ventilatory chemosensitivity. White Leghorn chicken eggs were incubated at 38 degrees C either in 21% O(2) (Controls) or in 15% O(2) for the whole 3-week incubation (HxTot) or for only the 1st (Hx1), 2nd (Hx2) or 3rd week of incubation (Hx3). Hatching time had a delay of half a day in HxTot, and was normal in the other groups. Body weight was similar in all hatchlings. Oxygen consumption ( [Formula: see text] ) and pulmonary ventilation (V e) were measured at about 20 h post-hatching. Ventilatory chemosensitivity was evaluated from the degree of hyperpnea (increase in V e) and hyperventilation (increase in [Formula: see text] ) during acute hypoxia (15 and 10% O(2), 20 min each) and acute hypercapnia (2 and 4% CO(2), 20 min each). The responses to hypoxia were similarly decreased in HxTot and in Hx3 compared to controls, and were normal in the other experimental groups; those to hypercapnia were blunted only in HxTot. The results are in agreement with the idea that prenatal hypoxia blunts V e chemosensitivity by interfering with the normal development of the carotid bodies.
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