title: Phospholipases A2 and platelet-activating-factor acetylhydrolase in patients with acute respiratory distress syndrome.
abstract: OBJECTIVE
  Phospholipases A2 (PLA2) comprise a family of enzymes probably implicated in the development of acute respiratory distress syndrome (ARDS). The aim was to investigate PLA2 activities and characteristics in bronchoalveolar lavage (BAL) fluid, BAL cells, and plasma from patients with ARDS by a fluorometric method.
  
  
  METHODS
  Prospective, controlled study.
  
  
  METHODS
  Fourteen-bed polyvalent intensive care unit in a university hospital.
  
  
  METHODS
  A total of 31 mechanically ventilated patients, 20 with and 11 without ARDS, were studied.
  
  
  METHODS
  BAL was performed by fiberoptic bronchoscopy in mechanically ventilated patients with a controlled mechanical ventilation mode.
  
  
  METHODS
  PLA2 and platelet-activating-factor acetylhydrolase were determined in BAL fluid, cells, and plasma. For the classification of PLA2-specific inhibitors, Western blot analysis and their biochemical characteristics were used.
  
  
  RESULTS
  In ARDS patients, increased PLA2 levels were detected in BAL fluid, BAL cells, and plasma compared with the control patients. PLA2 in BAL fluid was mainly type IIA secretory and cytosolic types. In plasma, type IIA secretory and cytosolic and a Ca-independent PLA2 were found. In BAL cells, a cytosolic form, probably a Ca-independent intracellular form, and a low activity of type IIA secretory PLA2 was also observed. Total PLA2 activity correlated inversely with Pao2/Fio2 ratio and positively with the mortality rate. Patients with direct ARDS exhibited higher PLA2 activity compared with patients with indirect ARDS. Platelet-activating-factor acetylhydrolase activity was higher in BAL fluid and plasma, but it was lower in BAL cells.
  
  
  CONCLUSIONS
  Ca-dependent, secretory, cytosolic, and Ca-independent forms of PLA2 and platelet-activating-factor acetylhydrolase could play important roles in the development or down-regulation of inflammation in ARDS, respectively.
authors.affiliation: Intensive Care Unit, University Hospital of Ioannina, Greece.
authors.forename: George
authors.initials: G
authors.lastname: Nakos
authors.forename: Eirini
authors.initials: E
authors.lastname: Kitsiouli
authors.forename: Eleana
authors.initials: E
authors.lastname: Hatzidaki
authors.forename: Vassilios
authors.initials: V
authors.lastname: Koulouras
authors.forename: Lhousseine
authors.initials: L
authors.lastname: Touqui
authors.forename: Marilena E
authors.initials: ME
authors.lastname: Lekka
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000378:metabolism*; D000109:Acetylcholine / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis; D015153:Blotting, Western; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002118:Calcium / Q000378:metabolism; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010741:Phospholipases A / Q000378:metabolism*; D054467:Phospholipases A2; D012128:Respiratory Distress Syndrome / Q000201:enzymology*; D016019:Survival Analysis
chemical_list: D015415:Biomarkers; D010741:Phospholipases A; D054467:Phospholipases A2; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000109:Acetylcholine; D002118:Calcium