Abstract：Objective Oxygen therapy is a common means in the treatment of lung disease in premature infants. However, long time inhalation of high concentration of oxygen can induce lung injury, even chronic lung disease (CLD). This paper aims at studying the dynamic changes of lung ultrastructure and oxidative stress reaction in premature rats with hyperoxia induced CLD and in exploring the role of lung oxidative stress reaction in pathogenesis of CLD. Methods Eighty premature rats were randomly assigned into a Hyperoxia group and a Control group (n=40 each). The Hyperoxia group was given a high concentration of oxygen (FiO 2>0.90) and developed CLD. The Control group received oxygen with the FiO 2 of 0.21. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration of the lung were assayed with a spectrophotometer and the lung ultrastructure in the two groups was observed under a transmission electronmicroscope. Results The structures of mitochondria and lamellar bodies in alveolar epithelial cell Ⅱ (AEC Ⅱ) were partly damaged on the 3rd day of hyperoxia induction. The abnormal nuclei developed in addition to the damaged mitochondria and lamellar bodies in AEC Ⅱ after the 7th day. Compared with the Control group, the MDA level in the Hyperoxia group was increased significantly on the 3rd day ( 55.9 ± 5.5 nmol/mg vs 22.5 ± 4.4 mmol/mg) (P< 0.01 ), and it reached a peak on the 7th day ( 94.3 ± 12.4 nmol/mg). After 7 days the MDA level in the Hyperoxia group decreased gradually but still remained at a higher level on the 21st day than that of the Control group ( 48.0 ± 7.5 nmol/g vs 23.6 ± 5.7 nmol/g) (P< 0.01 ). The SOD activity in the Hyperoxia group did not differ from the Control group. Conclusions AEC Ⅱ injury is early manifestation of hyperoxia induced CLD. The lung oxidative stress reaction is closely related to the AEC Ⅱ injury.
FU Jian-Hua,XUE Xin-Dong. Changes of ultrastructure and oxidative stress reaction of lungs in premature rats with
chronic lung disease induced by hyperoxia[J]. CJCP, 2004, 6(1): 23-26.
