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1 Department of Pediatrics, MetroHealth Medical Center, Cleveland, Ohio, USA
2 Department of Pediatrics, Rainbow Babies & Children's Hospital, Cleveland, Ohio, USA; Department of Medicine, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
3 Department of Pediatrics, Rainbow Babies & Children's Hospital, Cleveland, Ohio, USA
4 Department of Medicine, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA
* To whom correspondence should be addressed. E-mail: mmhanna{at}metrohealth.org.
Hyperoxic exposure enhances airway reactivity in newborn animals, possibly due to altered relaxation. We sought to define the role of prostaglandin and nitric oxide mediated mechanisms in impaired airway relaxation induced by hyperoxic stress. We exposed 7 day old rat pups to either room air or hyperoxia (>95% O2) for 7 days to assess airway relaxation and cAMP/cGMP production following electrical field stimulation (EFS). EFS-induced relaxation of preconstricted trachea was diminished in hyperoxic versus normoxic animals (p<0.05). Indomethacin (a cyclooxygenase inhibitor) reduced EFS-induced airway relaxation in tracheas from normoxic (p<0.05), but not hyperoxic rat pups, however, in the presence of L-NAME (a nitric oxide synthase inhibitor) EFS-induced airway relaxation was similarly significantly decreased in tracheas from both normoxic and hyperoxic animals. Following EFS the increase from baseline in the production of cAMP was significantly higher in tracheas from normoxic than hyperoxic rat pups, and this was accompanied by greater prostaglandin E2 (PGE2) release only in the normoxic group. cGMP production following EFS stimulation did not differ between normoxic and hyperoxic groups. We conclude that hyperoxia impairs airway relaxation in immature animals via a mechanism primarily involving the prostaglandi-cAMP signaling pathway with an impairment of PGE2 release and cAMP accumulation.
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