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1 Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA
2 Department of Pediatrics, San Antonio Military Pediatric Center, San Antonio, TX, USA
3 Department of Pediatrics, Southwest Foundation for Biomedical Research, San Antonio, TX, USA
4 Department of Pediatrics, San Antonio Military Pediatric Center, San Antonio, TX, USA; Department of Pediatrics, Southwest Foundation for Biomedical Research, San Antonio, TX, USA
* To whom correspondence should be addressed. E-mail: philip.shaul{at}utsouthwestern.edu.
Nitric oxide (NO), produced by NO synthase (NOS), serves multiple functions in the perinatal lung. In fetal baboons, neuronal (nNOS), endothelial (eNOS) and inducible NOS(iNOS) are all primarily expressed in proximal respiratory epithelium. In the present study, NOS expression and activity in proximal lung and minute ventilation of NO (VdotNOSTP) were evaluated in a model of chronic lung disease (CLD) in baboons delivered at 125d gestation (term = 185d) and ventilated for 14d, obtaining control lung samples from fetuses at 125d or 140d gestation. In contrast to the normal 73% increase in total NOS activity from 125 to 140d gestation, there was an 83% decline with CLD. This was related to marked diminutions in both nNOS and eNOS expression and enzymatic activity. nNOS accounted for the vast majority of enzymatic activity in all groups. The normal 3.3-fold maturational rise in iNOS protein expression was blunted in CLD, yet iNOS activity was elevated in CLD compared to at birth. The contribution of iNOS to total NOS activity was minimal in all groups. VdotNOSTP remained stable in the range of 0.5 to 1.0 nl/kg/min from birth to day of life 7, and it then rose by 2.5-fold. Thus, the baboon model of CLD is characterized by deficiency of the principal pulmonary isoforms, nNOS and eNOS, and enhanced iNOS activity over the first 2 weeks of postnatal life. It is postulated that these alterations in NOS expression and activity may contribute to the pathogenesis of CLD.
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