阻塞性睡眠呼吸暂停综合征模型大鼠心肌氧化应激的损伤及复氧后的变化

通过复制阻塞性睡眠呼吸暂停综合征（OSAHS）的间歇缺氧（IH）大鼠模型，观察IH对大鼠心肌氧化应激的损伤及其复氧后的变化情况。方法40 只SD 大鼠随机分为4 组，对照组（A 组）10 只，复制30只阻塞性睡眠呼吸暂停综合征的间歇缺氧大鼠模型，其中10 只缺氧组（B 组），10 只缺氧后复氧组（C 组），另外10 只持续缺氧组（D 组）。检测各组大鼠血清中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性，以及心肌组织中还原型谷胱甘肽（GSH）活性。结果与对照组大鼠比较，IH模型大鼠MDA 含量增高，SOD活性降低，心肌组织GSH 活性降低，差异具有统计学意义（ p<0.05）；复氧组大鼠MDA、SOD 和心肌组织GSH活性恢复正常，差异无统计学意义（ p>0.05）；而D 组大鼠MDA 含量增高，SOD 活性降低，心肌组织GSH 活性降低，差异具有统计学意义（p <0.05）。结论OSAHS 存在氧化应激，严重损伤心肌组织，缺氧时MDA 含量、SOD 和GSH 活性改变，复氧后有所恢复。血清MDA含量、SOD 活性及心肌组织GSH活性可以反应氧化应激的严重程度。

Myocardial oxidative stress injury and changes after reoxygenation in rat model of obstructive sleep apnea syndrome

To establish obstructive sleep apnea syndrome (OSAHS) rat model by intermittent hypoxia(IH) and to observe the myocardial oxidative stress injury and changes after reoxygenation. Methods In this study,10 untreated rats were enrolled into control group (group A). Through 30-d IH, obstructive sleep apnea syndrome model was established in 30 rats. among which 10 rats had examination of venous blood and myocardial tissues just after model establishment (group B), 10 rats had reoxygenation immediately after model establishment (group C) and their venous blood and myocardial tissues were examined after 30-d normal feeding, still 10 rats had IH for additional 30 days (group D) before examination of their venous blood and myocardial tissues. The content of serum malondialdehyde (MDA), the activity of serum superoxide dismutase (SOD), and the activity of glutathione (GSH) in myocardial tissue were detected and compared between the groups. Results Compared with the group A, the serum MDA content increased, the serum SOD activity and the activity of glutathione(GSH) in myocardial tissue decreased in the group B ( p< 0.05); the indexes returned to normal in the group C (p > 0.05); however, in the group D, the myocardial GSH activity and the serum SOD activity were significantly decreased, and the serum MDA content was significantly increased ( p< 0.05). Conclusions Oxidative stress appears in OSAHS, and causes severe injury ofmyocardial tissue. Hypoxia can change MDA content, and SOD and GSH activity which will recover after reoxygenation. Hence, serum MDA content and SOD and GSH activity can reflect the severity of oxidative stress in myocardial tissues.