Inhaled
nitric oxide (iNO) is a specific pulmonary
vasodilator. By serving as a
pro-oxidant or
antioxidant, iNO may influence other pulmonary functions as well. This study was designed to test the hypothesis that iNO affects the alveolar lining after
premature birth. Preterm rabbits (gestation 29 d, term 31 d) were nose-only exposed NO (14 ppm) and 98% O2, for 20 h. The others were exposed to either 98% O2 or air. In another experiment, premature rabbits were exposed to either NO in air or to air. After the exposure, bronchoalveolar lavage (BAL) was performed and the
surfactant aggregates were isolated. The
surfactant components and surface activity were analyzed. In total, 144 animals were studied. There were no significant differences in the number, distribution, or respiratory burst activity of cells recovered by BAL. Neither brief
hyperoxia nor iNO increased plasma-derived
proteins in BAL. Exposure to O2 decreased large
surfactant aggregates, surface activity, and the content of
surfactant protein B in BAL, whereas iNO prevented completely or partially these effects of acute
hyperoxia on
surfactant.
Hyperoxia increased the content of
malondialdehyde and decreased
glutathione in epithelial lining fluid. iNO decreased
malondialdehyde (p < 0.05) and tended to increase
glutathione (p = 0.06) in animals breathing O2.
Nitrotyrosine was not detectable in BAL, and NO2 was low in the breathing area. In room air, iNO had no significant effect on
surfactant. According to the present results, a brief period of
hyperoxia causes an
oxidant stress and decreases the surface activity of alveolar
surfactant in premature rabbits. In contrast, a low dosage of iNO decreased or prevented the O2-induced detrimental effects on alveolar
surfactant and alleviated the
oxidant stress.