Aim:To investigate the effects of inhaled nitric oxide(NO)on pulmonaryinflammation,apoptosis,peroxidation and protein nitration in a rat model of acutelung injury(ALI)induced by meconium.Methods:Twenty-four healthy maleSprague-Dawley rats were randomly devided into 3 groups(n=8):meconium-induced ALl with intratracheal instillation of 1 mL/kg saline(Mec/saline group),continuous inhalation of NO at 20 μL/L.(Mec/iNO),and the control group(control).Electromicroscopic examination was used to determine the extent of epithelialapoptosis.TUNEL was used to detect DNA fragmentation in pulmonary apoptoticcells,expressed as the apoptosis index(AI).Western blotting was used to detectpulmonary inducible NO synthase(iNOS)expression.RT-PCR was used to detectinterleukin(IL)-1β mRNA expression.Cell count in bronchoalveolar lavage(BAL),myeloperoxidase(MPO)activity,as well as malondialdehyde(MDA)andnitrotyrosine formation,the markers of toxic NO-superoxide pathway in rat lungparenchyma specimens,were also examined.Results:Expression of iNOS pro-tein and IL- 113 mRNA were increased significantly in the Mec/saline group(bothP<0.01)compared with the control group.BAL cell count,MPO activity,lunginjury score,pulmonary AI,MDA level and nitrotyrosine formation were alsoincreased significantly(all P<0.01).The meconium-induced iNOS protein andIL-1β mRNA expression were inhibited significantly by NO inhalation when com-pared with the Mec/saline group(both P<0.01 ).BAL cell count,MPO activity andlung injury score were also decreased significantly(P<0.01 or P<0,05).However,there were no statistical differences in MDA level,nitrotyrosine formation or pul-monary AI between the Mec/saline and Mec/iNO groups.Electromicroscopicexamination revealed a significant degree of epithelial apoptosis in both the Mec/saline and Mec/iNO groups.Conclusions:Early continuous inhalation of NO20 μL/L may protect the lungs from inflammatory injury,but does not decreaseepithelial apoptosis or lung nitrotyrosine formation.Inhalation of NO alone is notassociated with a detectable increase in oxidant stress. Aim: To investigate the effects of inhaled nitric oxide (NO) on pulmonary inflammation, apoptosis, peroxidation and protein nitration in a rat model of acute lung injury (ALI) induced by meconium. Methods: Twenty-four healthy male Sprague-Dawley rats were randomly devided into 3 groups (n = 8): meconium-induced ALI with intratracheal instillation of 1 mL / kg saline (Mec / saline group), continuous inhalation of NO at 20 μL / L ). Electromicroscopic examination was used to determine the extent of epithelialapoptosis. TUNEL was used to detect DNA fragmentation in pulmonary apoptotic cells, expressed as the apoptosis index (AI). Western blotting was used to detect pulmonary mRNA in NO synthase (iNOS) expression. RT-PCR was used to detect interleukin (IL) -1β mRNA expression. Cell count in bronchoalveolar lavage (BAL), myeloperoxidase (MPO) activity, as well as malondialdehyde (MDA) and nitrotyrosine formation, the markers of toxic NO- superoxide pathway in rat lung parenchyma specimens, were al so examined. Results: Expression of iNOS pro-tein and IL-113 mRNA were significantly increased in the Mec / saline group (bothP <0.01) compared with the control group.BAL cell count, MPO activity, lunginjury score, pulmonary AI, MDA level and nitrotyrosine formation were also significantly increased (all P <0.01). meconium-induced iNOS protein and IL-1β mRNA expression were significantly increased by NO inhalation when com-pared with the Mec / saline group (both P <0.01) There was no statistical differences in MDA level, nitrotyrosine formation or pul-monary AI between the Mec / saline and Mec / iNO (P <0.01 or P <0,05) groups. Electromicroscopicexamination revealed a significant degree of epithelial apoptosis in both the Mec / saline and Mec / iNO groups. Conclusions: Early continuous inhalation of NO20 μL / L may protect the lungs from inflammatory injury, but does not decreaseepithelial apoptosis or lung nitrotyrosine for mation.Inhalation of NO alone is not associated with a detectable increase in oxidant stress.