Reversibility of oxygen-induced injury to the alveolar epithelium: an ultrastructural study.

Continuous exposure of rabbits to 100% O2 at one atmosphere (1 ATA) for 48 h damages the alveolar epithelium increasing its permeability to lipid insoluble molecules. The purpose of this study was to quantify the reversibility of this injury upon resumption of air breathing, using a cytochemical technique. Rabbits were exposed to 100% O2 at 1 ATA for either 48 or 63 h and then returned to air. Cytochrome C (Cyt) was instilled into the alveolar space and detected ultrastructurally in the different components of the blood gas barrier by its peroxidase activity. After 63 h in 100% O2 and 24 h in air, Cyt was present in the basal lamina of all instilled alveoli. After 33 or 48 h in air, there was focal replacement of type I by type II pneumocytes. Cytochrome C was identified in the basal lamina of 30% of the alveoli lined with type I but not type II cells. In contrast, after 48 h in O2 followed by 24 h of breathing air, cytochrome C was totally restricted in the alveolar space. Our studies indicate that the increased alveolar permeability of the lung to Cyt abates completely 24 h after return to air. At this time, though, the PaO2 was significantly lower than control, indicating the existence of residual pulmonary damage. In contrast, the damage to the alveolar epithelium after 63 h of continuous O2 breathing is only partially restored, even after 48 h of return to room air.