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Chronic hyperoxia alters the hyperoxic ventilatory response and diaphragm muscle fiber composition in neonatal rats
Author(s) -
Heerden Eliza S,
Brackett Diane G,
Leso John I,
Dmitrieff Elizabeth F,
Bavis Ryan W
Publication year - 2011
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.25.1_supplement.1111.5
Subject(s) - hyperoxia , diaphragm (acoustics) , ventilation (architecture) , myosin , chemoreceptor , hypoxic ventilatory response , medicine , endocrinology , respiratory system , biology , lung , microbiology and biotechnology , receptor , mechanical engineering , physics , acoustics , loudspeaker , engineering
We recently reported that normoxic ventilation is decreased in neonatal rats following chronic hyperoxia (4–7 d in 60% O 2 ), and that this is only partially explained by reduced metabolic demand (Bavis et al. J Appl Physiol 109: 796–803, 2010). The present study considered whether decreased respiratory drive from peripheral chemoreceptors and/or abnormal development of the diaphragm might contribute to this plasticity. Rats were exposed to 60% O 2 from birth until studied at 4, 6–7, or 13–14 d of age. Normoxic ventilation, measured by head‐body plethysmography, was significantly reduced at P4 and P6–7 in hyperoxia‐treated rats, but not at P13–14. The acute ventilatory response to 99% O 2 was reduced at P4 and P6–7 as well, suggesting a diminished contribution of carotid chemoreceptors to normoxic ventilation. Diaphragm fiber types were investigated by immunohistochemistry. Overall, a greater proportion of muscle fibers from hyperoxia‐treated rats expressed the embryonic myosin heavy chain (MHC) isoform, particularly at P4. Together, these observations suggest multiple mechanisms by which chronic hyperoxia might compromise eupneic ventilation. Supported by NIH grant HL‐083972.