Inhaled steroid therapy has potential advantages over systemic steroid of fewer side effects and direct delivery to the target tissue in the treatment of bronchopulmonary dysplasia(BPD). Hyperoxia may produce lung injury and inactivation of surfactant by the generation of free radical. Inhaled steroid therapy may reduce lung inflammation and potentially the incidence of BPD. We hypothesized that budesonide may protect surface active properties of PS in neonatal rats with hyperoxic exposure. To clarify this, newborn rats were exposed to 95% oxygen and administered budesonide(Pulmicort®, ASTRA, Sweden) by ultrasonic nebulizer for 24 hour in an air-tight box(H+B group, n=13). Control rats(n=13) were exposed to 95% oxygen (H group, n=13) and room air (R group, n=7). After euthanizing animals, we incised trachea and performed lavage. We obtained the part containing the surfactant from the lavage fluid by differential centrifuge. Pulsating Bubble Surfactometer(Electronetics, NY) was used to measure adsorption rate and in vitro minimum and maximum surface tensions(ST). Results are 1) H group had higher adsorption rate than R and H+B group. 2) The maximum ST after 5 min of pulsation were similar among 3 groups. The minimum ST after 5 min of pulsation increased significantly in H group than in R and H+B group. Conclusively, in budesonide-treated newborn rats exposed to hyperoxia, surface tension was lower than those exposed to hyperoxia without the treatment. Thus, we demonstrated that budesonide has a protective effect in hyperoxia-induced inactvation of surfactant. *p<0.05 compared to R and H+B, **p<0.001 compared to R and H+B. Values are mean±SD Table

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