The pulmonary injury in rats caused by chronic intermittent hypoxia and the intervention effect of Edaravone

To investigate the mechanism of the pulmonary injury in rats caused by chronic intermittent hypoxia (CIH) and to investigate the intervention effect of Edaravone.Ninety-six male Wistar rats were divided into four groups randomly: the control group (NC), chronic intermittent hypoxia group (CIH), chronic intermittent hypoxia normal saline matched group (NS), chronic intermittent hypoxia edaravone treatment group (NE). The four groups were also divided into 1, 2, 3, 4 W time subgroups, and each time subgroup had 6 rats. After the experiment, sections of pulmonary were stained with hematoxylin-eosin (HE) and the level of SOD, MDA, PO2 and Ang II mRNA 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, 2, 3, 4 W. But the pulmonary histology of the UC group and the NS group was normal. Compared with the NS group, pulmonary injury of NE group 1, 2, 3, 4 W, significantly decreased. Compared with the NC group, the levels of PO2 in the CIH group were decreased; while the compared with the NS group, the levels of PO2 in the NE group were increased. Compared with the UC group and NS group, the levels of Ang II mRNA in each time point in CIH group were increased gradually (P < 0.05), the content of MDA were increased in 1, 2, 3, 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 NS group; The Ang II mRNA levels of CIH in pulmonary showed positive correlation with MDA [r = 0.782,P < 0.01]; while the Ang II mRNA levels of CIH in pulmonary showed negative correlation with SOD [r = - 0.904, P < 0.01].CIH can cause pulmonary injury through oxidative stress and activating Ang II, and Edaravone could prevent pulmonary injury induced by CIH through scavenging oxygen free radicals.