Background: Contributing factors in bronchopulmonary dysplasia (BPD) in neonatal infants includes inflammation and oxygen radicals. Nitric oxide (NO - 2), an important mediator of inflammation can lead to cell injury or induce proinflammatory cytokines. Glucocorticoids are known to decrease the transcription of inducible NO synthetase. Objective: To investigate if there are altered serum (NO 2) nitrite, a products of NO metabolism levels in very low birth weight infants with BPD and respiratory distress syndrome (RDS) as compared to healthy newborns before and after dexamethasone treatment. Methods: We clinically evaluated neonatal infants and obtained samples from 31 infants diagnosed with BPD (N=15), RDS (N=6), prematurity without respiratory distress syndrome (N=6), and full term (FT) neonates (N=4). Levels of nitrite were measured using the Greiss Reagent, and absorbance was determined at 550nm. Results: The highest levels of NO- 2 were obtained in the BPD patients (9-253 μM), mean = 110 μM, with low APGAR scores at 1 minute from 0 to 5. RDS patients with low APGAR scores at 1 minute from 5 to 7, also had high levels (8-93 μM), mean=54 μM and patients with prematurity with normal APGAR scores at 1 minute from 6 to 9 had relatively low NO- 2 levels (29-76 μM), mean = 41mM. Dexamethasone treatment (0.5 mg/kg/d) of 12 hrs. for 3-8 days) in premature infants with low APGAR scores dramatically decreased from 85-253 μM to 10-146μM (p < 0.05). In 2 of the severe BPD a rise in NO levels after dexamethasone correlated with severe systemic infection. NO - 2 levels in FT patients (21 - 37μM), (mean=30 μM). Control serum samples from 16 infants randomly selected had NO levels of (8-53 μM), mean = 28 μM). Supported by a fellow-in-training grant* and Von Pirquet Awardsd from ACAAI.