Linked Life Data

12736380

Source:http://linkedlifedata.com/resource/pubmed/id/12736380

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-7-25
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0031-3998
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
185-91
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Endogenous surfactant metabolism in newborn infants with and without respiratory failure.
pubmed:affiliation
Division of Newborn Medicine, St. Louis Children's Hospital, 1 Children's Place, St. Louis, MO 63110, U.S.A.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't