[Changes of angiotensin II and oxidation stress during the development of chronic intermittent-induced pulmonary injury in rats].

To observe the changes of angiotensin II and the levels of oxidation stress during the development of chronic intermittent hypoxia(CIH)-induced pulmonary injury in rats, and the effect in the mechanism of CIH-induced pulmonary injury.Seventy-two male Wistar rats were divided into three groups: control group (UC), sham control group (SC) and chronic intermittent hypoxia group (CIH). The three groups were also divided into 1 w, 2 w, 3 w, 4 w time subgroups, and each time subgroup has 6 rats. UC rats were not treated, The CIH rats were subjected to alternating cycles of nitrogen and compressed air, while SC rats were similarly treated but received compressed air instead of nitrogen. After the experiment, sections of pulmonary were stained with hematoxylin-eosin (HE) and the level of SOD, MDA, Ang II and AngIImRNA in rat homogenate pulmonary were measured.Pulmonary histology revealed that the CIH group showed high levels of interstitial edema, alveolar atelectasis, inflammatory cell infiltration of alveolar epithelial cell, pulmonary injury were serious in 1 w, 2 w, 3 w, 4 w. But the pulmonary histology of the NC group and the SC group was normal. Compared with the UC group and SC group, the expression of angiotensin II (AngII) protein, the levels of AngIImRNA in each time point in CIH group were increased gradually (P<0.05), the content of MDA were increased in 1 w, 2 w, 3 w, 4 w (P<0.05), they had reached the peak all at 4 w; while the SOD in each time point in CIH group were decreased gradually (P<0.05) compared with that in UC group and SC group; the AngII and AngIImRNA levels of CIH in pulmonary showed positive correlation with MDA (r= 0.751, 0.782, P<0.01); while the AngIIand AngⅡmRNA levels of CIH in pulmonary showed negative correlation with SOD [r=-0.743, -0.904, P<0.01].CIH can activate oxidation stress and AngII, which were mutually causal and maybe an important mechanism of CIH-induced pulmonary injury.