Surfactant Phosphatidylcholine Metabolism in Severe Neonatal Lung Disease: Studied with Stable Isotopes

Abstract

Avery and Mead showed in 1959 that pulmonary surfactant deficiency is a major factor in the pathophysiology of respiratory distress syndrome (RDS). In 1980 Fujiwara et al. administered exogenous surfactant for the first time successfully to preterm infants with RDS (2). This was followed by numerous clinical trials that demonstrated a decrease in death rates and complications. There are now accumulating data which suggest that a disturbed surfactant metabolism plays a role in several other neonatal lung diseases, such as congenital diaphragmatic hernia (CDH), meconium aspiration syndrome (MAS), surfactant protein-B (SP-B) deficiency, and neonatal pneumonia and/or sepsis. Also in adult respiratory distress syndrome, asthma, infectious lung diseases, and interstitial lung diseases. Insufficient surfactant function could be due to a disturbance in surfactant kinetics or secondary to an inactivation of surfactant by several components. Surfactant therapy possibly plays a therapeutical role in the management of these clinical conditions. This review will focus on the surfactant metabolism in term neonatal lung diseases. We will discuss the role of surfactant in CDH, MAS, SP-B deficiency, and neonatal pneumonia and/or sepsis. First, we will briefly review the functions and composition of surfactant and the normal cellular metabolism of surfactant.