Pulmonary surfactant plays an important role in alveoli to lower surface tension. It is well known that lecithin, a main component of surfactant, is synthesized from fatty acids at type II alveolar cell. Beta 2 receptor mediated secretion also has been postulated. Recently the existence of surface active substance in the E-tube has been reported. The chemical composition and surface tension lowering properties were found to be almost identical in both pulmonary and E-tube surfactants. However synthetic process and secretory mechanism of E-tube surfactant have not been studied extensively and never been observed in conjunction with pulmonary surfactant. Radioisotope tagged 3H-palmitic acid was infused into auricular vein of 47 New Zealand white rabbits and hourly radioactivity was measured from both pulmonary and E-tube lavage fluids in order to quantitate synthesis and secretion of surfactant. Radioactivities of lavage fluid from both lung and E-tube increased gradually and continuously and revealed the highest value at 15 hours after infusion. The rise and fall patterns of radioisotope activities were similar in both pulmonary and E-tube lavage fluid, but overall amount was much higher in pulmonary lavage fluid. Thin layer chromatographic analysis of both lavage fluids demonstrated phospholipid as main component. Injection of beta 2-receptor agonist, terbutaline, caused markedly increased radioisotope activites in both lavage fluids and also showed increased amount of phospholipid on thin layer chromatographic analysis of both lavage fluids. Phosphatidylcholine fraction of phospholipid was much higher in terbutaline treated group, and higher in pulmonary lavage fluid than in E-tube lavage fluid. In conclusion, the pulmonary and E-tube surfactants were similar in synthesis and secretion patterns, and terbutaline stimulates not only the secretion of pulmonary surfactant but also E-tube surfactant.