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  • Title: Endogenous surfactant metabolism in newborn infants with and without respiratory failure.
    Author: Bohlin K, Merchak A, Spence K, Patterson BW, Hamvas A.
    Journal: Pediatr Res; 2003 Aug; 54(2):185-91. PubMed ID: 12736380.
    Abstract:
    Studies using stable isotopically labeled glucose and palmitate as precursors of pulmonary surfactant synthesis have demonstrated slow surfactant turnover in premature infants with respiratory distress syndrome (RDS). However, only limited data about surfactant turnover are available for term infants. Because acetate is a direct precursor of de novo synthesized surfactant fatty acid, we measured [1-13C1]acetate incorporation into surfactant of term infants without respiratory dysfunction (control group), preterm infants with RDS, and term infants with primary respiratory failure to determine whether stable isotopically labeled acetate would yield similar results to previous studies of preterm infants with RDS and, furthermore, would distinguish normal from abnormal surfactant turnover. Despite similar amounts of phospholipids and acetate precursor enrichment, the control group had higher fractional synthetic rate and shorter half-life of clearance than preterm infants with RDS, (fractional synthetic rate, 15.4 +/- 2.4 versus 2.2 +/- 0.4%/d, p < 0.001; half-life of clearance, 27 +/- 3 versus 105 +/- 11 h, p < 0.001). Term infants with severe respiratory failure had a lower fractional synthetic rate than those with mild disease (2.9 +/- 0.6 versus 13.8 +/- 3.5%/d, p = 0.014) and a reduced amount of phospholipids recovered from tracheal aspirates (54 +/- 17 versus 300 +/- 28 nmol, severe versus mild disease, respectively, p < 0.001). The amount of phospholipids in tracheal aspirates correlated inversely with disease severity, (r = -0.75, p = 0.01). We conclude that normal surfactant turnover in term infants is faster than in preterm infants with RDS. Surfactant turnover in term infants with severe respiratory failure is similar to that of preterm infants with RDS, suggesting either delayed maturity of the surfactant system or disruption from the underlying disease process.
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