血管内皮生长因子在模拟高原缺氧小鼠脑组织、心肌组织中的表达研究

目的 研究血管内皮生长因子（VEGF）在模拟高原缺氧小鼠脑和心肌组织中的表达及意义.方法采用低压氧舱模拟海拔8000 m高原缺氧环境,将BALB/c小鼠随机分为正常对照组,缺氧6 h组、9 h组、12 h组、24 h组、2 d组、3 d组,每组10只.HE染色切片观察缺氧不同时间小鼠脑组织和心肌组织的组织病理学改变情况,免疫组织化学法检测脑组织和心肌组织VEGF蛋白的表达水平差异及其规律.结果 缺氧各组脑组织血管周、神经细胞周和胶质细胞周间隙扩大,细胞核染色质不均匀,呈空泡状或网状,脑组织间质内空泡状结构增多;心肌组织轻度血管扩张充血,细胞轻度肿胀,横纹消失结构不清呈均质状,少量肌细胞核固缩深染.缺氧各组脑、心肌组织VEGF阳性表达强度半定量评分较正常对照组显著增加（P＜0.01）,且随缺氧时间延长表达增加.结论 缺氧能造成小鼠脑和心肌组织损伤,呈现水肿病理表现,并刺激VEGF分泌,导致新生血管形成.

Expressions of Vascular Endothelial Growth Factor on the Brain and Myocardial Tissues of Mice in Mimical High-altitude Hypoxic Environment

Objective To research expressions and significance of vascular endothelial growth factor （VEGF） on the brain and myocardial tissues of mice in mimical high-altitude hypoxic enviroment. Methods Hypobaric chambers were used in simulation of an environment of 8000 meters high altitude environment, and BALB/c mice were randomly di- vided into normal control group, hypoxia for 6 h, 9 h, 12 h, 24 h, 2 d and 3 d groups （n = 10）. Pathological changes of brain and myocardial tissues in different hypoxia times were observed by using the HE staining; the VEGF protein ex- pression levels and its rules of brain and myocardial tissues were also detected by using immunohistochemical method. Results Interspaces among blood vessels, nerve cells and glial cells in brain tissues of each group expanded, nuclear chromatin was uneven with vacuolization or reticulation, vacuole interstitial structures were increased in the brain tissues ; mild vascular dilatation and congestion, mild swelling of part muscle cells, the disappearing transverse striations with un- clear structures and deeply stained homogeneous shape with a small amount of muscle karyopyknosis were found in myo- cardial tissues. Compared with that in normal brain and myocardial tissues, the semi-quantitative scores of VEGF positive expression of hypoxia groups significantly increased （ P 〈 0.01 ）, and the expressions increased with prolonged hypoxia time. Conclusion Hypoxia can cause damages of brain and heart tissues with pathological edema in mice, and can stim- ulate VEGF secretion and induce the neovascularization.