间歇性缺氧及睡眠剥夺建立大鼠睡眠呼吸暂停模型

目的建立睡眠呼吸暂停综合征（SAS）大鼠模型。方法选取雄性SD大鼠32只，随机分为4组，分别是常氧正常睡眠对照组，常氧睡眠剥夺组，间歇性低氧正常睡眠组，间歇性低氧睡眠剥夺组，每组8只。实验期间每周测定鼠尾收缩压1次，在缺氧、睡眠剥夺终点测定有创动脉压、心脏重量（CW），左心室重量（LVW），并计算出心脏质量指数（CMI）；取大动脉、肺、肾组织石腊包埋，病理切片光镜观察。结果随时间的延长，睡眠剥夺组、间歇性低氧组、间歇性低氧睡眠剥夺组鼠尾压逐步升高，并出现左室重量、心脏重量增加，以间歇性低氧睡眠剥夺组最为明显；组织病理显示低氧睡眠剥夺组大鼠动脉壁不规则增厚，肾小管上皮细胞肿胀，可见蛋白管型；肺小动脉管壁增厚，管腔变窄。结论通过模拟间歇性缺氧及睡眠剥夺机制建立了大鼠睡眠呼吸暂停综合征动物模型。

Establishment of Sleep Apnea Syndrome Model in Rats with Intermittent Hypoxia and Sleep Deprivation

Objective To establish a sleep apnea syndrome （SAS） model in rats. Methods Thirty two male Wistar rats were randomly divided into four groups： the control group, sleep deprivation group, intermittent hypoxia group, intermittent hypoxia and sleep deprivation group. The experiment lasted for 8 weeks, during the experiment, tail-cuff systolic blood pressure was measured everyweek. At the end of the experiment, invasive arterial blood pressure was measured and the cardiac and left ventricular were weighed. The Cardiac Mass Index was estimated. Tissues from the large artery, lungs and kidneys were embedded in paraffin and histological examination was conducted. Results During various intervals of intermittent hypoxia exposure or sleep deprivation, tail-cuff systolic blood pressure progressively increased. At end of the experiment, both the cardiac weight, left ventricular weight and invasive arterial blood pressure also increased, especially the intermittent hypoxia and sleep deprivation group. Compared with the control group, the arterial vascular wall, as well as the pulmonary arteriole vascular wall of rats in the intermittent hypoxia and sleep deprivation group became thicker. At the same time, epithelial cells of renal tubules showed typical hydropic degeneration and protein cast appeared in the renal tubules. Conclusion A sleep apnea syndrome rat model was successfully established by intermittent hypoxia exposure and sleep deprivation.