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Extracts of normal lung have been shown to contain a surface active agent that by decreasing alveolar surface tension serves to stabilize the alveoli during respiration (1-3). This surfactant has been shown to contain lipid probably complexed with protein (4, 5). Several investigators have suggested that the lipid is primarily dipalmitoyl lecithin [L-a-(dipalmitoyl) glycerophosphoryl choline], a highly surface active phospholipid (5-7). Increased surface tension in lung extracts occurs in certain disease states associated with respiratory distress (2). In man these states include the respiratory distress syndrome of infancy and oxygen toxicity. A similar respiratory distress syndrome can be produced experimentally in dogs and rabbits by exposure to increased oxygen tension. In both clinical and experimental situations respiratory distress, pulmonary edema, and atelectasis are associated with increased pulmonary surface tension (8-10). Our purpose in the present experiment was to induce changes in pulmonary surface tension in dogs by exposure to increased oxygen tension, to remove pulmonary surfactant by endobronchial lavage, and to measure lipid composition and surface activity. Endobronchial lavage rather than lung mincing was utilized to obtain alveolar surface lipids free of whole lung lipids, since previous studies had shown that whole lung lipids differ markedly from those of the alveolar surface (11).

Alterations in pulmonary surface active lipids during exposure to increased oxygen tension.