Developmental plasticity of the hypoxic ventilatory response after perinatal hyperoxia and hypoxia

Both genetic and environmental factors influence the normal development of the respiratory control system. This review examines the role perinatal O 2 plays in the development of normoxic breathing and the hypoxic ventilatory response in mammals. Hyperoxia and hypoxia elicit plasticity in respirator...

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Bibliographic Details
Published in:Respiratory physiology & neurobiology 2005-11, Vol.149 (1), p.287-299
Main Author: Bavis, Ryan W.
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Carotid body
Development
Humans
Hyperoxia
Hyperoxia - physiopathology
Hypoxia
Hypoxia - physiopathology
Infant, Newborn
Plasticity
Respiratory Mechanics - physiology
Respiratory System - growth & development
Respiratory System - physiopathology
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Summary:Both genetic and environmental factors influence the normal development of the respiratory control system. This review examines the role perinatal O 2 plays in the development of normoxic breathing and the hypoxic ventilatory response in mammals. Hyperoxia and hypoxia elicit plasticity in respiratory control that is unique to development and may persist weeks to years after return to normoxia. Specifically, both hyperoxia and hypoxia during early postnatal development attenuate the adult hypoxic ventilatory response, but the underlying mechanisms for this plasticity differ. Hyperoxia attenuates the hypoxic ventilatory response through potentially life-long changes in carotid body function. Neonatal hypoxia appears to have short-term effects on carotid body function, but persistent changes in the hypoxic ventilatory response may instead reflect changes in respiratory mechanics or related neural pathways. Overall, it appears that a relatively narrow range of environmental O 2 is consistent with “normal” postnatal respiratory control development, predisposing animals to potentially maladaptive plasticity in the face of disease or atypical environmental conditions.
ISSN:1569-9048
1878-1519
DOI:10.1016/j.resp.2005.04.003