摘要
目的建立大鼠睡眠呼吸暂停综合征(SAS)动物模型。方法选取Wistar雄性青年大鼠与老年大鼠各30只。各组分为常氧对照组及间歇性缺氧组,每组6只。实验中抽取气体用于气体成分分析,测氧仪监测吸入气氧浓度,在缺氧终点测定右室肥厚指数、右室压力以了解缺氧对右心的影响;取肺、肾组织石腊包埋,病理切片,光镜观察。结果①随缺氧时间延长,出现右室肥大、肺动脉高压。②肺组织学观察:肺血管壁增厚、肺泡间隔增宽;肾小管上皮水肿变性。结论通过模拟间歇性缺氧机制成功建立大鼠睡眠呼吸暂停综合征动物模型。
Objective To establish a sleep apnea syndrome （SAS） animal model in rats. Methods Young （3 months of age, weighing 250 ± 30 g） and old （20 months of age,weighing 450 ± 50 g） male Wistar rats were divided into the control group and intermittent hypoxia exposure group. Each group was divided into five sub - groups with varying time durations of hypoxia exposure （group control, IH 1 w, IH2 w, IH 4w and IH 12w, n = 6）. Gas samples were collected from the cabin for gas analysis. At end of the experiment, right ventricular pressure was measured and the weight of right and left ventricles was measured. The ratio of right ventricular weight to ventricular weight （right ventricular hypertrophy index） was estimated. Tissues from the lungs and kidneys were embedded in paraffin and histological analysis was carried out. Results 1. During various intervals of intermittent hypoxia exposure, both blood pressure and right ventricular hypertrophy index of rats were progressively increased. At end of the experiment, both young and old rats displayed pulmonary artery hypertension. Statistical analysis showed significant differences between the IH 12 w groups and the control group （ P 〈 0.01） . 2. Compared with the control group, both young and old Wistar rats in the IH 4 w and IH 12 w groups displayed right ventricular hypertrophy （P 〈 0.05）. 3. Pneumoangiogram showed increased thickness of the vascular wall and pulmonary alveoli were microscopically extensively changed. 4. Epithelial cells of renal tubules showed typical hydropic degeneration. Conclusion A sleep apnea syndrome rat model can be successfully generated by intermittent hypoxia exposure.
出处
《中国实验动物学报》
CAS
CSCD
2006年第1期40-43,T0004,共5页
Acta Laboratorium Animalis Scientia Sinica
基金
中央保健局专项资金资助(编号:渝A040)
