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1 Department of Pediatrics, University of Texas Health Science Center, San Antonio, TX, USA
2 Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA
3 Department of Medicine, National Jewish Medical and Research Center, Denver, CO, USA
4 Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA
5 Department of Pathology, University of Texas Health Science Center, San Antonio, TX, USA; Southwest Foundation for Biomedical Research, San Antonio, TX, USA
6 Department of Pediatrics, San Antonio Military Pediatric Center, San Antonio, TX, USA
7 Department of Pediatrics, University of Utah Health Sciences Center, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: philip.shaul{at}utsouthwestern.edu.
Nitric oxide (NO) serves multiple functions in the developing lung, and pulmonary NO production is decreased in a baboon model of chronic lung disease (CLD) after premature birth at 125d gestation (term = 185d). To determine if postnatal NO administration alters the genesis of CLD, the effects of inhaled NO (iNO, 5 ppm) were assessed in the baboon model over 14d. iNO caused a decrease in pulmonary artery pressure in the first 2d and a greater rate of spontaneous closure of the ductus arteriosus, and lung compliance was greater and expiratory resistance was improved during the first week. With iNO, postmortem pressure-volume curves were shifted upwards, lung DNA content and cell proliferation were increased, and lung growth was preserved to equal that which occurs during the same period in utero. In addition, the excessive elastin deposition characteristic of CLD was normalized by iNO, and there was evidence of stimulation of secondary crest development. Thus, in the baboon model of CLD, iNO improves early pulmonary function and alters lung growth and extracellular matrix deposition. As such, NO biosynthetic pathway dysfunction may contribute to the pathogenesis of CLD.
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