Jingjing Qi1, Wenlin Yao2, Qiangyong Kou2, Jing Wang2, Feng Chen2, Ming Fang2, *
1Department of Respiratory and Critical Care Medicine, Xiangzhou District People's Hospital, Xiangyang, 441000, China - 2Xiangzhou District People's Hospital, Xiangyang, 441000, China
Introduction: Chronic lung diseases are most often caused by the inhalation of excessive oxygen by premature infants. Chronic lung diseases in my country's premature infant population show a yearly increasing trend. Chronic lung diseases have become the diseases that seriously affect the lives and health of premature infants. Studies have shown that the pathogenesis of chronic lung disease is closely related to ultrastructural changes of the lung and to the oxidative stress response. The purpose of this article is to evaluate hyperoxia-induced chronic lung disease in premature rats, including existing problems and the specific effects of the hyperoxia-induced oxidative stress response.
Methods: We recruited 30 premature infants who were divided into a control group and an observation group for chronic lung disease. A high-oxygen environment was used to create a model of chronic lung disease in premature rats. We detected changes in the activity of peroxide and superoxide in the lung tissue of premature rats and observed the lung ultrastructure, recorded the experimental data, and carried out statistical analysis.
Results: The results of the study showed that the superoxide dismutase activity index in lung tissue increased from the base 85.36±4.7 to 126.57.2±5.9 after inhalation of an excessively high concentration of oxygen by the premature rats, and the activity index of peroxide malondialdehyde increased from the base 187.28±6.64 to 241.86±7.23; furthermore, the lung tissue of premature rats was damaged and the ultrastructure of the lung cells was also damaged, to a certain extent.
Conclusion: Excessive inhalation of high-concentration oxygen can induce the destruction of lung cell ultrastructure in premature rats and increase the oxidative stress response in the lungs, thereby causing chronic lung disease.
Hyperoxia induction, chronic lung disease, lung ultrastructure changes, oxidative stress response.