Blood gas tension and development of lung damage in mice exposed to oxygen at 1 ATA

Oxygen and carbon dioxide tension in arterial blood were studied in mice breathing 100% oxygen at ambient pressure. The lungs were simultaneously investigated in order to relate the oxygen-induced pulmonary alterations to the altered pulmonary function. The development of an impairment in pulmonary diffusing capacity is initiated after 30 h of oxygen exposure, at which time the increase in lung weight is associated with beginning lung edema and beginning accumulation of carbon dioxide in the blood. Red spots or areas on the lung surface, which merged together to large streaks or areas after 20 h of exposure, preceded the measurable diffusing impairment noted at 30 h. Light microscope preparations revealed intraalveolar hemorrhagic exudation and proliferative changes in the alveolar walls. After 50 h, the development of severe pulmonary dysfunction is mainly due to an intense parenchymal reaction in the alveolo-capillary region with thickening in the alveolar walls, dystelectasis in the corresponding parenchyma, and further development of pulmonary edema. The resulting impairment in pulmonary diffusing capacity causes a steep decrease in oxygen tension and an accentuated increase in carbon dioxide accumulation. The present results are discussed in relation to the previous findings of oxygen-induced alterations in brain glutamate, GABA, and glutamine concentration.