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.