Surfactant metabolism in neonatal lung diseases

Abstract

Pulmonary surfactant reduces surface tension in the lungs to impressive low values. When secreted by the type II cells into the thin liquid layer that lines the alveolar air spaces, vesicles of pulmonary surfactant absorb readily to the air water interface and form an interfacial film. The surfactant unique tensioactive properties were originally explained by its unique phospholipid composition, which is strikingly comparable across species [1]. Of the surfactant lipids, 80–90% are phospholipids, of which phosphatidylcholine (PC) is quantitatively the most important, accounting for 70–80% of the total. Other lipids include phosphatidylglycerol (PG), phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine, sphingomyelin, cholesterol, triacylglycerols, and free fatty acids. Approximately 60% of the PC contains two saturated fatty acids (DSPC) of which dipalmitoyl (16:0/16:0; DPPC) is the most abundant. DPPC and PG are key phospholipids that permit normal breathing by reducing surface tension to near zero at the end of the respiratory cycle.