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J Appl Physiol (October 17, 2003). doi:10.1152/japplphysiol.00825.2003
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Submitted on August 4, 2003
Accepted on October 9, 2003

Chronic O2 Exposure in the Newborn Rat Results in Decreased Pulmonary Arterial Nitric Oxide Release and Altered Smooth Muscle Response to Isoprostane

Jaques Belik1*, Robert P Jankov1, Jingyi Pan1, Ma Yi1, Imran Chaudhry1, and Allan K Tanswell1

1 Pediatrics, University of Toronto, Toronto, Ontario, Canada

* To whom correspondence should be addressed. E-mail: Jaques.Belik{at}sickkids.ca.

Chronic oxygen exposure in the newborn rat results in lung isoprostane formation, which may contribute to the pulmonary hypertension evident in this animal model. The purpose of this study was to investigate the pulmonary arterial smooth muscle responses to 8-iso-prostaglandin F2{alpha} (8-iso-PGF2{alpha}) in newborn rats exposed to 60% O2 for 14 days. Since, in the adult rat, 8-iso-PGF2{alpha} may have a relaxant effect, mediated by nitric oxide (NO), we also sought to evaluate the pulmonary arterial NO synthase (NOS) protein content and NO release in the newborn exposed to chronic hyperoxia. Compared to air-exposed control animals, 8-iso-PGF2{alpha} induced a significantly greater force (P<0.01) and reduced (P<0.01) relaxation of pre-contracted pulmonary arteries in the 60% O2-treated animals. These changes were reproduced in control pulmonary arteries by NOS blockade using LNAME. Pulmonary arterial endothelial was unaltered, but the inducible NOS protein content was significantly decreased (P<0.01) in the experimental group. Pulmonary (P<0.05) and aortic (P<0.01) tissue ex vivo NO accumulation was significantly reduced in the 60% O2 treated animals. We speculate that impaired pulmonary vascular tissue NO metabolism following chronic O2 exposure potentiates 8-iso-PGF2{alpha}-induced vasoconstriction in the newborn rat, thus contributing to pulmonary hypertension.




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