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Chronic hyperoxia alters the early and late phases of the hypoxic ventilatory response in neonatal rats
Author(s) -
Bavis Ryan W,
Young Kristen M,
Barry Kevin J,
Boller Matthew R,
Kim Eugene,
Klein Peter M,
Ovrutsky Alida R,
Rampersad Donna A
Publication year - 2009
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.23.1_supplement.621.15
Subject(s) - hyperoxia , hypoxic ventilatory response , ventilation (architecture) , carotid body , medicine , plethysmograph , hypoxia (environmental) , room air distribution , respiratory minute volume , control of respiration , respiratory system , anesthesia , endocrinology , lung , oxygen , chemistry , stimulation , mechanical engineering , physics , organic chemistry , engineering , thermodynamics
Perinatal hyperoxia causes long‐lasting attenuation of the hypoxic ventilatory response (HVR) in rats, but the timing of these ventilatory changes has not been investigated during the hyperoxic exposure. Rats were raised in room air (control) or 60% O 2 from birth until studied at 4, 6‐7, and 13‐14 days of age. Ventilation was measured by head‐body plethysmography in 21% O 2 and in 12% O 2 . Normoxic ventilation was significantly reduced at P4 and P6‐7 in hyperoxia‐treated rats, which may be partially explained by lower metabolic rates. Control rats exhibited a biphasic HVR at P4 and P6‐7; the secondary decline diminished with advancing age and was no longer observed by P13‐14. Hyperoxia‐treated rats exhibited a sustained increase in ventilation at all ages, however, suggesting that hyperoxia hastens postnatal maturation of the central components of the HVR. The early (carotid body‐mediated) phase of the HVR tended to be greater in hyperoxia‐treated rats relative to controls at P4 (P=0.09 at minute 1) but decreased as the hyperoxic exposure progressed (i.e., significantly reduced at P6‐7 and P13‐14 vs. controls). Thus, it appears that short exposures to chronic hyperoxia initially enhance the HVR but that this is gradually overcome by impaired carotid body function. Supported by NIH grant R15 HL‐083972.