中文摘要：

目的观察、探讨肺泡Ⅱ型细胞凋亡在急进高原大鼠肺损伤中的作用与意义。方法 60只wistar大鼠急进高原后,随机分高原1、3、7 d组,经处理,观察大鼠肺组织大体形态变化;H-E染色,显微镜观察肺组织学变化,电镜观察肺组织超微结构的变化。结果光镜下,大鼠肺组织出现了明显的炎症反应,肺泡壁毛细血管充血水肿,肺泡腔内有大量炎细胞;电镜下,肺泡上皮细胞凋亡明显。实验组形态学损伤重于对照组,且细胞凋亡率高于对照组,两者存在统计学差异（P〈0.05）。结论急进高原大鼠Ⅱ型细胞凋亡可能是引起高原急性肺损伤的原因之一,推测凋亡可能导致肺水转运障碍、钠水潴留而引发肺损伤。但其肺水转运障碍引发肺损伤的作用机制还有待于进一步研究。

英文摘要：

Objective To observe the significance of AT ⅡI cell apoptosis in rats in the early stage of acute lung injury at high altitude. 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 with H - E staining. Electron microscope was used to observe the uhrastructural changes in the lung tissue. Results There were significant inflammatory reaction in pulmonary tis- sue, alveolar wall blood capillary hyperemia and edema under light microscope. Under electron microscope, the ap- optosis was shown in alveolar epithelium ceils obviously. The morphological damage of experimental group is serous than that of positive group, and the rate of apoptosis of positive group was lower than that of negative group. There was significant difference （P 〈 0.05 ）. Conclusions The AT Ⅱ cell apoptosis in rats at highland may be one cause of acute lung injury, apoptosis may lead to lung water transport barriers and then accumulated in alveoli and cause pul- monary edema eventually, But the lung water transport barrier induced lung injury remains to be further studied.