title: Induced hypernatraemia is protective in acute lung injury.
abstract: BACKGROUND
  Sucrose induced hyperosmolarity is lung protective but the safety of administering hyperosmolar sucrose in patients is unknown. Hypertonic saline is commonly used to produce hyperosmolarity aimed at reducing intra cranial pressure in patients with intracranial pathology. Therefore we studied the protective effects of 20% saline in a lipopolysaccharide lung injury rat model. 20% saline was also compared with other commonly used fluids.
  
  
  METHODS
  Following lipopolysaccharide-induced acute lung injury, male Sprague Dawley rats received either 20% hypertonic saline, 0.9% saline, 4% albumin, 20% albumin, 5% glucose or 20% albumin with 5% glucose, i.v. During 2h of non-injurious mechanical ventilation parameters of acute lung injury were assessed.
  
  
  RESULTS
  Hypertonic saline resulted in hypernatraemia (160 (1) mmol/l, mean (SD)) maintained through 2h of ventilation, and in amelioration of lung oedema, myeloperoxidase, bronchoalveolar cell infiltrate, total soluble protein and inflammatory cytokines, and lung histological injury score, compared with positive control and all other fluids (p ≤ 0.001). Lung physiology was maintained (conserved PaO2, elastance), associated with preservation of alveolar surfactant (p ≤ 0.0001).
  
  
  CONCLUSIONS
  Independent of fluid or sodium load, induced hypernatraemia is lung protective in lipopolysaccharide-induced acute lung injury.
authors.affiliation: Dept of Critical Care Medicine, Flinders University, Adelaide, Australia; Intensive and Critical Care Unit, Flinders Medical Centre, Adelaide, Australia. Electronic address: biharishailesh@gmail.com.
authors.forename: Shailesh
authors.initials: S
authors.lastname: Bihari
authors.affiliation: Dept of Critical Care Medicine, Flinders University, Adelaide, Australia; Intensive and Critical Care Unit, Flinders Medical Centre, Adelaide, Australia. Electronic address: dani.dixon@flinders.edu.au.
authors.forename: Dani-Louise
authors.initials: DL
authors.lastname: Dixon
authors.affiliation: Dept of Critical Care Medicine, Flinders University, Adelaide, Australia. Electronic address: mark.lawrence@flinders.edu.au.
authors.forename: Mark D
authors.initials: MD
authors.lastname: Lawrence
authors.affiliation: Dept of Critical Care Medicine, Flinders University, Adelaide, Australia; Intensive and Critical Care Unit, Flinders Medical Centre, Adelaide, Australia. Electronic address: andrew.bersten@flinders.edu.au.
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Bersten
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D004195:Disease Models, Animal; D006955:Hypernatremia / Q000473:pathology / Q000503:physiopathology; D008070:Lipopolysaccharides; D008168:Lung / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D008297:Male; D045283:Natriuretic Agents / Q000008:administration & dosage* / Q000494:pharmacology; D020011:Protective Agents / Q000008:administration & dosage* / Q000494:pharmacology; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D015656:Respiratory Mechanics / Q000187:drug effects / Q000502:physiology; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage* / Q000494:pharmacology*; D016896:Treatment Outcome
chemical_list: D008070:Lipopolysaccharides; D045283:Natriuretic Agents; D020011:Protective Agents; D012462:Saline Solution, Hypertonic
keywords: Fluids; Hypernatraemia; Hypertonic saline; LPS lung injury model; Lung injury; Lung oedema