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Published online before print October 18, 2006
Eur Respir J 2006, doi:10.1183/09031936.00016106
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ORIGINAL ARTICLE

Alterations of exhaled nitric oxide in preterm infants with chronic lung disease

H.L. Roiha 1, C.E. Kuehni 2, M. Zanolari 1, M. Zwahlen 2, D.N. Baldwin 1, C. Casaulta 1, M. Nelle 1, U. Frey 1*

1 Swiss Paediatric Respiratory Research Group, Department of Paediatrics, University Hospital of Berne, Switzerland
2 Swiss Paediatric Respiratory Research Group, Department of Social and Preventive Medicine, University of Berne, Switzerland

* To whom correspondence should be addressed. E-mail: urs.frey{at}insel.ch.


  Abstract

Animal models suggest that reduced nitric oxide synthase (NOS) activity results in lower values of exhaled NO (eNO) present at birth in those individuals who are going to develop chronic lung disease of infancy (CLDI).

We measured on-line tidal eNO in 39 unsedated preterm infants with CLDI (mean gestational age GA 27.3 weeks) in comparison to 23 healthy preterm (31.6 weeks) and 127 term infants (39.9 weeks) at 44 weeks postconceptional age, thus after the main inflammatory response. We calculated NO output (V'NO=eNO*flow) to account for tidal flow related changes. We controlled for sex, maternal atopic disease and environmental factors (smoking, caffeine).

Mean eNO was not different (14.9 ppb in all groups), but V'NO was lower in CLDI compared to healthy term infants (0.52 vs. 0.63 nL·s-1, p=0.024). Values for healthy preterms were between these two groups (0.58 nL·s-1). Within all preterms (n=62), V'NO was reduced in infants with low GA, high CRIB scores and longer duration of oxygen therapy, but not associated with postnatal factors such as ventilation or corticosteroids.

After accounting for flow, the lower NO output in premature infants with CLDI is consistent with the hypothesis of NO metabolism being involved in CLDI.

Keywords:  Chronic lung disease, infants, lung function, nitric oxide, prematurity




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