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Time‐dependent alterations in peripheral chemoreceptor activity during postnatal hyperoxia
Author(s) -
Bavis Ryan W,
Donnelly David F
Publication year - 2008
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.22.1_supplement.1224.7
Subject(s) - hyperoxia , carotid body , chemoreceptor , hypoxia (environmental) , peripheral chemoreceptors , anesthesia , peripheral , medicine , endocrinology , electrophysiology , chemistry , oxygen , lung , receptor , organic chemistry
Postnatal hyperoxia, as low as 30% O 2 and lasting 1–4 weeks, attenuates the ventilatory response to acute hypoxia due to profound impairment of peripheral chemoreceptors. The present study investigated the time course of this impairment by recording single‐unit chemoreceptor action potentials (APs) following 1, 3, 5, 8 and 14 days of hyperoxia treatment. Rat pups were placed in hyperoxia (60% O 2 ) at P7. Pups were then removed at P8, P10, P12, P15 and P21 and single‐unit activities were isolated and recorded in vitro from the soma of petrosal neurons with projections to the carotid body. Compared with chemoreceptors of normoxia‐reared pups, hyperoxia enhanced the peak‐discharge response to acute hypoxia after 1 day of hyperoxia. In contrast, the peak‐discharge response was significantly reduced by 5 days of hyperoxia and remained low for the duration of the treatment period. Conduction time for an AP to progress from the carotid body to petrosal ganglion was also lengthened by the fifth day of hyperoxia treatment. Because nerve conduction time lengthens with the same time course as changes in the acute response to hypoxia, it suggests that at least some of the response impairment is due to changes in afferent nerve excitability characteristics. Supported by NIH grants P20 RR‐016463 (Maine INBRE) and HL‐073500.