Crapo J D, Barry B E, Foscue H A, Shelburne J
Am Rev Respir Dis. 1980 Jul;122(1):123-43. doi: 10.1164/arrd.1980.122.1.123.
The lungs of rats exposed to 100% O2 until death and to 85% O2 for as long as 14 days were studied using morphometric and biochemical techniques. The primary injury leading to death in rats exposed to 100% O2 was injury to the pulmonary capillary endothelium, where 44% of the endothelial cells were destroyed; there was a corresponding decrease in capillary surface area and in capillary lumen volume. Animals exposed to 85% O2 had proliferation and hypertrophy of alveolar Type II epithelial cells. In addition, 41% of the capillary endothelial cells were destroyed, but the endothelial cells that survived 7 days in 85% O2 were hypertrophied, and after this point no further destruction of the pulmonary capillary bed took place. Exposures to 85% O2 led to enhanced activity of the copper-zinc and manganese superoxide dismutases, which might be related to the apparently adaptive structural changes that occurred in the alveolar Type II epithelium and in the capillary endothelial cells.
运用形态学和生物化学技术，对暴露于100%氧气直至死亡以及暴露于85%氧气长达14天的大鼠肺部进行了研究。暴露于100%氧气的大鼠导致死亡的主要损伤是肺毛细血管内皮损伤，其中44%的内皮细胞被破坏；毛细血管表面积和管腔容积相应减少。暴露于85%氧气的动物出现肺泡II型上皮细胞增生和肥大。此外，41%的毛细血管内皮细胞被破坏，但在85%氧气环境中存活7天的内皮细胞肥大，此后肺毛细血管床未再发生进一步破坏。暴露于85%氧气导致铜锌超氧化物歧化酶和锰超氧化物歧化酶活性增强，这可能与肺泡II型上皮细胞和毛细血管内皮细胞中发生的明显适应性结构变化有关。
