title: Altered platelet-activating factor levels and acetylhydrolase activities are associated with increasing severity of bronchopulmonary dysplasia.
abstract: Lipid inflammatory mediators are thought to play an important role in the pathogenesis of neonatal lung injury and bronchopulmonary dysplasia (BPD). Because preliminary studies from the intensive care nursery of the University of Tennessee Medical Center, Knoxville, revealed linear increased in blood platelet-activating factor (PAF) levels in very low birthweight infants developing chronic lung disease and lower cord blood PAF acetylhydrolase activities in premature infants, it was theorized that altered platelet-activating factor levels and PAF acetylhydrolase activities are associated with increasing severity of BPD. Platelet-activating factor levels (blood and tracheal lavage) and PAF acetylhydrolase activities (blood and tracheal lavage) were measured over days 1 to 2, 3 to 5 and 6 to 7 in 16 ventilated infants and weekly in 9 infants with bronchopulmonary dysplasia. Platelet-activating factor values were normalized per nanogram of lavage blood urea nitrogen. Severity of bronchopulmonary dysplasia was estimated using the scoring system developed by Toce. Mean blood and lavage PAF levels and PAF acetylhydrolase activities were compared in infants developing bronchopulmonary dysplasia with those without the disease over the first seven days of life. Infants developing chronic lung disease were significantly smaller and of younger gestational age. In infants with bronchopulmonary dysplasia, higher PAF levels in blood were seen on days 3 to 5, along with increased lavage acetylhydrolase activities on days 1 to 2. Increased levels of PAF in lavage on days 3 to 5 were associated with increasing severity of bronchopulmonary dysplasia. Altered blood and lavage platelet-activating factor levels and PAF acetylhydrolase activities appear to be associated with the pathogenesis and severity of bronchopulmonary dysplasia.
authors.affiliation: Department of Pediatrics, University of Tennessee Graduate School of Medicine, Knoxville 37920, USA.
authors.forename: M S
authors.initials: MS
authors.lastname: Gaylord
authors.forename: Z L
authors.initials: ZL
authors.lastname: Smith
authors.forename: V
authors.initials: V
authors.lastname: Lorch
authors.forename: M L
authors.initials: ML
authors.lastname: Blank
authors.forename: F
authors.initials: F
authors.lastname: Snyder
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000328:Adult; D015415:Biomarkers; D001997:Bronchopulmonary Dysplasia / Q000097:blood*; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D008297:Male; D010741:Phospholipases A / Q000097:blood*; D010972:Platelet Activating Factor / Q000378:metabolism*; D011379:Prognosis
chemical_list: D015415:Biomarkers; D010972:Platelet Activating Factor; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase