Mechanisms of Structural-Functional Defects in Pulmonary Oxygen Toxicity.

摘要

The means by which hyperbaric oxygen causes pulmonary damage is being studied at the ultrastructural and molecular biological level. The effect of increased oxygen concentrations on the metabolic and synthetic acitvities of the pulmonary alveolar component with special emphasis on tis synthesis of surfactant,and how this may relate to adaptation to high pO2levels has been a primary concern of this project. Studies of synthesis of RNA during increased pO2have shown a reversible inhibition of overall RNA synthesis. A more specific inhibition of ribosomal-RNA processing,which leads eventually to cell death since new protein synthesis is blocked,has been detected and would account for fatal O2toxicity resulting from prolonged exposure. Studies attempting to elucidate the mechanism of tolerance or adaptation to a toxic O2environment have demonstrated proliferation of alveolar type II cells and an increase in overall pulmonary phospholipid synthesis including surfactant.