Premium
Hypoxic ventilatory response of rats after intermittent hypercapnic hyperoxia and intermittent hyperoxia
Author(s) -
Simons Julia C.,
Russell Kate E.R.,
Bavis Ryan W.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1213-b
Subject(s) - hyperoxia , hypercapnia , hypoxic ventilatory response , hypoxia (environmental) , carotid body , anesthesia , ventilation (architecture) , plethysmograph , chemoreceptor , respiration , medicine , room air distribution , peripheral chemoreceptors , endocrinology , respiratory system , oxygen , lung , chemistry , stimulation , anatomy , mechanical engineering , physics , receptor , organic chemistry , engineering , thermodynamics
Perinatal hyperoxia attenuates the hypoxic ventilatory response in adult rats by impairing carotid body development. We hypothesized that this plasticity is caused by hyperoxic inhibition of chemoreceptor activity during development. Thus, we predicted that the effects of hyperoxia on the hypoxic ventilatory response could be reduced by stimulating chemoreceptors with periods of CO 2 during hyperoxia or by interrupting hyperoxia with periods of normoxia. Rats were born and raised in 60% O 2 for the first two postnatal weeks. One group was simultaneously exposed to intermittent hypercapnia (alternating 1‐h exposures to 0 and 7.5% CO 2 ) while another group was only exposed to intermittent hyperoxia (alternating 1‐h exposures to 21 and 60% O 2 ). Hypoxic ventilatory responses were measured at 6–8 weeks of age by whole‐body barometric plethysmography. Rats exposed to intermittent hypercapnia during hyperoxia exhibited 89% greater increases in ventilation‐to‐metabolism ratio (V E /V O2 ) in response to 12.5% O 2 than rats exposed to only hyperoxia (P=0.04), while rats exposed to intermittent hyperoxia exhibited 70% greater V E /V O2 responses than rats exposed to hyperoxia alone (P=0.04). These data support the hypothesis that activity‐dependent mechanisms contribute to hyperoxia‐induced developmental plasticity. Further, these data suggest a role for activity‐dependent mechanisms in normal development of the hypoxic ventilatory response. Supported by a Howard Hughes Medical Institute grant to Bates College.