Pulmonary surfactant, a mixture of phospholipid and protein, stabilizes lungs by lowering surface tension and preventing alveolar collapse at end expiration. Respiratory distress syndrome (RDS) in infants most commonly results from a quantitative deficiency of pulmonary surfactant after premature birth (1,2). Nutrition may affect the composition and function of pulmonary surfactant (3). It is unclear if preformed fatty acids or de novo synthesized fatty acids are utilized preferentially in preterm infants for surfactant phospholipid synthesis. Recently developed methods utilizing naturally occurring, stable, non-radioactive isotope labeled metabolic precursors of phospholipid synthesis provide the opportunity to understand possible influences on surfactant metabolism in infants (4-7). We will use intravenous infusions of surfactant phospholipid precursors ( [1,2,3,4-13C4] palmitate and [1-13C1] acetate) and gas chromatography/mass spectrometry (GC/MS) to test the hypothesis that: plasma palmitate is utilized preferentially for surfactant synthesis in preterm infants less than 28 weeks gestational age. The respective rates of acetate and palmitate incorporation into the surfactant of preterm infants will be compared. The use of labeled metabolic precursors of surfactant phospholipid provides a unique and powerful approach in the evaluation of surfactant metabolism.
| Spence, Kimberly L; Zozobrado, James C; Patterson, Bruce W et al. (2005) Substrate utilization and kinetics of surfactant metabolism in evolving bronchopulmonary dysplasia. J Pediatr 147:480-5 |
