Abstract
The lung is the primary target organ for normobaric oxygen toxicity. In addition, pulmonary bacterial infection is a frequent complication of prolonged oxygen therapy. A progressive, dose-related deterioration in pulmonary antibacterial defense mechanisms was induced in 215 laboratory mice by exposure to oxygen tensions of 650 mm Hg for 12, 24, 48, 72 and 96 hr. An additional 65 mice, maintained in atmospheric air (oxygen tension: 140 mm Hg), were used as controls. An aerosol inoculum of radiotracer tagged (32P) Staphylococcus aureus (FDA 209P, type 42D) was delivered to oxygen treated and control animals for 30 min. The animals were