The pulmonary surfactant most likely functions as a surface film which upon compression during expiration prevents alveolar collapse. The surfactant is probably expended by being irreversibly excluded from the alveolar surface film at the time of maximal film compression at end-expiration. A deficiency of pulmonary surfactant is associated with atelectasis and respiratory failure, although the factors which control surfactant synthesis and secretion are unknown. Saturated phosphatidylcholine (SPC) is the most important and the largest single component of the pulmonary surfactant. Lung phosphatidylcholine de novo synthesis has been shown to be inversely related to functional parameters such as surface area, respiratory rate or sigh frequency. This has suggested a functional relationship between the synthesis of lung PC and factors which affect the alveolar lining layer. We propose to investigate the relationship of three basic factors to the synthesis of DSPC, pulmonary histologic, surface tension and pressure-volume relationships. The three factors are: 1. ventilation (Dogs), 2. hibernation (Bats), 3. lung development (Rats).