title: Sevoflurane, but not propofol, reduces the lung inflammatory response and improves oxygenation in an acute respiratory distress syndrome model: a randomised laboratory study.
abstract: BACKGROUND
  Acute respiratory distress syndrome is characterised by activation of the inflammatory cascade. The only treatment that reduces the mortality rate associated with this syndrome is lung protective ventilation, which requires sedation of patients. Sedation in critical care units is usually induced intravenously, although there is reason to believe that inhaled anaesthetics are a suitable alternative. Sevoflurane has recently been shown to modulate the lung inflammatory response in a model of lung injury more favourably than propofol.
  
  
  OBJECTIVE
  The goal of this study was to confirm whether or not sevoflurane is more effective than propofol in ameliorating the inflammatory response in an animal model of acute respiratory distress syndrome.
  
  
  METHODS
  A prospective, randomised, controlled study.
  
  
  METHODS
  Research foundation laboratory at the Hospital Clínico Universitario, Valencia, Spain.
  
  
  METHODS
  Sixteen Landrace/large white crossbred pigs weighing 30 to 45 kg.
  
  
  METHODS
  Animals were allocated randomly to one of two groups: one sedated with intravenous propofol 5 to 7 mg kg h (group P) and the other with sevoflurane, administered using an AnaConDa device to obtain an end-tidal concentration of 1.5% (group S). Monitoring, lung protective ventilation and anaesthetic management were identical in both groups.
  
  
  METHODS
  The PaO2/FiO2 ratio and cytokine concentrations in bronchoalveolar lavage specimens were determined at 10, 150 and 240 min after confirmation of acute respiratory distress syndrome (PaO2/FiO2 <26.7 kPa).
  
  
  RESULTS
  At 240 min, median and interquartile range (IQR) concentrations of cytokines in bronchial lavage specimens in group S were lower than those in group P [interleukin-1β (IL-1β) 53, IQR 16-140 vs. 311, IQR 183-637 pg ml, P = 0.04; tumour necrosis factor-α 347, IQR 161-433 vs. 552, IQR 475-649 pg ml, P = 0.04; and IL-6 101, IQR 76-282 vs. 580, IQR 369-701 pg ml, P = 0.03]. The polymorphonuclear neutrophil count was also lower in group S (P = 0.007), which also had a higher PaO2/FiO2 ratio.
  
  
  BACKGROUND
  GE-015/09.
  
  
  CONCLUSIONS
  In an animal model of acute respiratory distress syndrome, sevoflurane ameliorates the lung inflammatory response and improves oxygenation to a greater extent than propofol.
authors.affiliation: Department of Anesthesiology and Intensive Care, Fundación de Investigación (INCLIVA), Hospital Clínico Universitario de Valencia, Valencia, Spain.
authors.forename: Carlos
authors.initials: C
authors.lastname: Ferrando
authors.forename: Gerardo
authors.initials: G
authors.lastname: Aguilar
authors.forename: Laura
authors.initials: L
authors.lastname: Piqueras
authors.forename: Marina
authors.initials: M
authors.lastname: Soro
authors.forename: Joaquin
authors.initials: J
authors.lastname: Moreno
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Belda
mesh_terms: D000758:Anesthesia / Q000379:methods; D018685:Anesthetics, Inhalation / Q000627:therapeutic use; D000818:Animals; D002463:Cell Membrane Permeability; D004195:Disease Models, Animal; D006439:Hemodynamics; D007249:Inflammation / Q000188:drug therapy*; D007262:Infusions, Intravenous; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D008738:Methyl Ethers / Q000627:therapeutic use*; D016343:Monitoring, Intraoperative; D009504:Neutrophils / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism*; D015742:Propofol / Q000627:therapeutic use*; D011897:Random Allocation; D012128:Respiratory Distress Syndrome / Q000188:drug therapy*; D000077149:Sevoflurane; D013552:Swine; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D018685:Anesthetics, Inhalation; D008738:Methyl Ethers; D000077149:Sevoflurane; D010100:Oxygen; D015742:Propofol