Abstract • 118

Bronchopulmonary dysplasia (BPD) is a complex disorder of infants with intermittent wheezing. Hyperoxia, inflammation and oxygen radicals are contributing factors. Nitric oxide (NO) as an important mediator of inflammation via toxic radicals can initiate cell injury or induce pro-inflammatory cytokines, and we previously described NO induction of IL-8 in human tracheal epithelial cells (Am J Respir Crit Care Med, 15:642a, 1995). We clinically evaluated neonatal infants and obtained serum samples for NO from 21 infants diagnosed with BPD (N=8), respiratory distress syndrome (RDS) (N=3), prematurity without respiratory disease (N=6), or full-term (FT) neonates (N=4). Levels of NO were measured using the Greiss reagent, and the absorbance was determined at 550 nm. The highest levels of NO were observed in the BPD patients (68-253 µM) with a high severity index and low apgar score. RDS patients with low apgar scores also had high NO levels (66-93 µM, Mean = 78 µM), whereas patients with prematurity with normal apgar scores had relatively low NO levels (11-46 µM, Mean = 27.6 ± 15.4). Dexamethasone treatment (0.5 mg/kg/day, every 12 hrs for 8 days) in 3 premature infants with low apgar scores dramatically decreased NO levels from 160 ± 113µM - 56.8 ± 77 µM p + <.05). NO levels in FT patients ranged from 21 to 37 µM (Mean = 30 µM). Control serum samples from 16 infants randomly selected without evaluation for BPD and RDS had NO levels from 8 to 53 µM (Mean = 27.6 ± 13.2 µM). Thus, NO levels in neonates with BPD and RDS coincided with disease severity, lower apgar scores, and might be utilized as an inflammatory biomarker for oxidant injury or used for monitoring treatment with corticosteroids.