Surfactant metabolism in the neonate

Abstract

With the use of stable isotope-labeled intravenous precursors for surfactant phosphatidylcholine (PC) synthesis, it has been shown that the de novo synthesis rates in preterm infants with respiratory distress syndrome (RDS) are very low as are turnover rates. This is consistent with animal data. Surfactant therapy does not inhibit endogenous surfactant synthesis, and prenatal corticosteroids stimulate it. With the use of stable isotope-labeled PC given endotracheally, surfactant pool size was estimated. It turned out to be low in RDS, as expected. Similar studies were performed in term neonates with severe lung diseases. In general, patients with lung injury show a lower surfactant synthesis. The controversy around surfactant in congenital diaphragmatic hernia (CDH) persists: studies on CDH with and without extracorporeal membrane oxygenation yielded different results. In severe meconium aspiration syndrome surfactant synthesis was found to be decreased but surfactant pool size was maintained. It is possible and safe to study surfactant metabolism in human neonates with the use of stable isotopes. This can help in answering clinical questions and has the potential to bring new in vitro and animal findings about surfactant metabolism to the patient.