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Departments of 1Pediatrics and 5Pathology, University of Texas Health Science Center; 6The Southwest Foundation for Biomedical Research; 7San Antonio Military Pediatric Center, San Antonio; 4Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas; 2Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri; 3Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; and 8Department of Pediatrics, University of Utah Health Sciences Center, Salt Lake City, Utah
Submitted 16 September 2004 ; accepted in final form 14 November 2004
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 125 days (d) gestation (term = 185d). To determine whether 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 upward, 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.
nitric oxide; patent ductus arteriosus
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