Based on these metabolic studies of surfactant lipids in term lambs, in preterm lambs not treated with surfactant, and in preterm lambs that have been surfactant-treated, the following is a synthesis of the overall metabolism of surfactant. Preterm surfactant-deficient lungs seem to have all the synthetic and secretory pathways for surfactant phosphatidylcholine. Secretory kinetics are slow in preterm relative to term animals. Recycling pathways are active in the preterm lung, and surfactant used for treatment can be recycled. The major difference between the preterm or term lung and the adult lung is that there is almost no surfactant phosphatidylcholine catabolism in the developing lung. All assessments of surfactant metabolism are complicated by the different forms of surfactant within the airspaces that represent different functional surfactant pools. SP-A has secretory and reuptake kinetics quite different than those for phosphatidylcholine. De novo synthesized SP-A is secreted independently of lamellar bodies and may associate with surfactant lipids during the formation of tubular myelin. Surfactant treatments do not adversely affect endogenous synthetic and secretory phospholipid pathways by feedback inhibition. Therefore, surfactant treatments have two primary effects on the preterm lung: physiological effects related to surface properties, and metabolic effects resulting from the exogenous surfactant phospholipids functioning as substrate for the recycling pathways.