ATⅡ细胞在急性高原肺水肿中的作用和意义.docVIP

ATⅡ细胞在急性高原肺水肿中的作用及意义 　　作者：吴岳,赵海龙,马祁生,田育璋,胥谨　　作者单位：1.青海大学医学院 ; 2.中山大学护理学院 　　【摘要】 目的 探讨ATⅡ细胞在急性高原肺水肿中的作用及意义。方法 wister大白鼠随机分高原1 d、3 d、7 d组，观察肺组织大体形态变化;H-E染色，观察肺组织学变化;电镜观察肺组织形态学变化;测定血流动力学和右室肥厚指数(RVHI)。结果 光镜下，肺组织出现明显炎症反应，肺泡壁充血水肿，肺泡腔内有大量的炎细胞;电镜下，肺泡上皮细胞出现凋亡。血流动力学测定、右室肥厚指数测定结果显示表明：1 d、3 d和7 d组mPAP 、mSAP和RVHI变化无显著性差异(P0.05)。结论 缺氧使ATⅡ细胞凋亡，肺水转运功能障碍，肺泡内液体大量聚集，从而引发肺水肿。 　　【关键词】 高原环境 肺组织 凋亡 肺水肿 　　Abstract Objective To investigate the morphological and hemodynamic changes of pulmonary tissues in Wister rats under plateau environment and provide enlightenment for clarifying the mechanism of high altitude pulmonary edema. Methods To divide the Wister rats into 3 groups (1d,3d and 7d) at plateau randomly and to observe the morphological changes of pulmonary tissue. The mean pulmonary arterial pressure (mPAP), mean systematic arterial pressure (mSAP) and the right ventricle hypertrophy index were detected simultaneously. Results There were significant inflammatory reactions in pulmonary tissue. Congestion and edema were shown in pulmonary alveoli wall and a great amount of inflammatory cells presented in alveolar space under microscope. The apoptosis was shown in alveolar epithelium cells under electron microscope. The detection of hemodynamic and RVHI showed that there were no significant differences among 1d, 3d and 7d groups of mPAP, mSAP and RVHI (P0.05). Conclusion Hypoxia leads to the ATⅡ cell apoptosis and hindrance to the pulmonary water transportation and then accumulated in alveoli and cause pulmonary edema eventually. 　　Key words Plateau environment Pulmonary tissues Apoptosis Pulmonary edema 　　高原肺水肿(high altitude pulmonary edema, HAPE)是一种严重的急性高原病，一般是由低海拔地区急速进入海拔2500 m以上地区时因低氧而引起[1]。它的临床表现与一般急性肺水肿相似：呼吸困难、咳嗽、咳大量白色或粉红色泡沫痰，听诊示两肺布满湿啰音[2]。高原肺水肿的发病机制现在尚不清楚，早期学者将其描述为肺炎或充血性心力衰竭。目前较为公认的学说认为高原肺水肿是一种高蛋白，高渗出性肺水肿[3]，但其具体原因不是很清楚。本实验采用高原现场实验观察方法，探讨ATⅡ细胞在急性高原肺水肿中的作用及意义。 　　1 材料与方法 　　1.1 材料 　　健康Wistar大鼠60只，鼠龄6～8周，体重210～230 g，由青海省实验动物中心提供。随机分成3组(1d、3d、7d组)。选择海拔