Davis W B, Rennard S I, Bitterman P B, Crystal R G
N Engl J Med. 1983 Oct 13;309(15):878-83. doi: 10.1056/NEJM198310133091502.
To study the early changes in the lower respiratory tract in persons exposed to periods of hyperoxia usually considered safe, we evaluated 14 normal subjects by bronchoalveolar lavage before and immediately after 16.7 +/- 1.1 hours of breathing more than 95 per cent oxygen. Hyperoxia caused a significant alveolar-capillary "leak" as detected by the presence of increased plasma albumin and transferrin in lavage fluid. These changes were reversible, as shown at repeat lavage in four subjects two weeks after oxygen administration. Hyperoxia for an average of 17 hours did not change the total number or type of lung inflammatory and immune effector cells recovered by lavage (P greater than 0.05, all comparisons). However, alveolar macrophages from subjects exposed to oxygen released increased amounts of fibronectin (P less than 0.05) and alveolar-macrophage--derived growth factor for fibroblasts (P less than 0.01)--mediators thought to modulate fibroblast recruitment and proliferation in the alveolar wall. Thus, although some of the effects of exposure to 17 hours of more than 95 per cent oxygen are reversible, hyperoxia for even this short period lowers the structural or functional barriers that normally prevent alveolar-capillary "leak" and induces processes that can culminate in fibrosis of the alveolar wall.
为了研究暴露于通常认为安全的高氧环境中的人群下呼吸道的早期变化，我们在14名正常受试者呼吸超过95%氧气16.7±1.1小时之前和之后立即通过支气管肺泡灌洗进行评估。通过灌洗液中血浆白蛋白和转铁蛋白增加可检测到，高氧导致了显著的肺泡-毛细血管“渗漏”。这些变化是可逆的，如在4名受试者吸氧两周后重复灌洗所示。平均17小时的高氧并未改变通过灌洗回收的肺部炎症和免疫效应细胞的总数或类型（所有比较中P均大于0.05）。然而，暴露于氧气的受试者的肺泡巨噬细胞释放了更多的纤连蛋白（P小于0.05）和成纤维细胞的肺泡巨噬细胞衍生生长因子（P小于0.01），这些介质被认为可调节成纤维细胞在肺泡壁中的募集和增殖。因此，尽管暴露于95%以上氧气17小时的一些影响是可逆的，但即使在这么短的时间内，高氧也会降低通常防止肺泡-毛细血管“渗漏”的结构或功能屏障，并诱导可能最终导致肺泡壁纤维化的过程。
