Pulmonary oxygen toxicity. Connective tissue changes during injury and repair

Our results show early decreased lung hydroxyproline content and increased urinary hydroxyproline excretion following oxygen exposure. The contribution of collagen from the lung to total urinary hydroxyproline excretion is not known. However, since the lung is the organ most damaged under normobaric hyperoxia, we assume that the increased urinary hydroxyproline excretion found in the oxygen-exposed group is derived from the lung. Excretion data were not conclusive concerning degradation of lung elastin. We conclude that the early decreased lung hydroxyproline content and increased hydroxyproline excretion indicate degradation of lung collagen. We hypothesize that the subsequent rapid deposition (indicated by increased lung hydroxyproline content) of functionally abnormal fibers results in the emphysema-like changes found after recovery from oxygen toxicity in rats.