title: Hypothermia protects against endotoxin-induced acute lung injury in rats.
abstract: OBJECTIVE
  Hypothermia in humans and animals is known to decrease the number and function of circulating neutrophils. Because an activation of circulating neutrophils and their sequestration into the lung are important pathogenetic phenomena in endotoxin-associated lung injury, we conjectured that hypothermia could prevent this type of lung injury.
  
  
  METHODS
  Animal study at a university-affiliated research institute.
  
  
  METHODS
  Thirty-six Sprague-Dawley rats.
  
  
  METHODS
  After anesthesia, the rats were randomly assigned to normothermia (37 degrees C, rectal temperature) or hypothermia (27 degrees C), which was induced by surface cooling. After 1 h of stable temperature, the rats were administered intratracheal doses of lipopolysaccharide (LPS; 3 mg/kg) (normothermia-LPS; hypothermia-LPS) or an equivalent volume of normal saline (normothermia-saline; hypothermia-saline). The rectal temperature was maintained within +/-1 degrees C of the target temperature for 6 h after the intratracheal treatment.
  
  
  RESULTS
  Compared with the normothermia-LPS group, the neutrophil count in bronchoalveolar lavage (BAL) fluid (p=0.002) and the myeloperoxidase activity of lung tissues (p=0.002) of the hypothermia-LPS group were both lower. Compared with the normothermia-LPS group, the BAL interleukin-1beta level of the hypothermia-LPS group was lower (p<0.001), whereas the BAL interleukin-10 level of the hypothermia-LPS group was higher (p=0.026). Compared with the normothermia-LPS group, the histologic scores for acute lung injury of the hypothermia-LPS group were lower (p=0.007).
  
  
  CONCLUSIONS
  Hypothermia pretreatment decreased the pulmonary sequestration of neutrophils, induced a favorable balance between pro- and anti-inflammatory cytokines, and attenuated histologic injury in endotoxin-challenged rats.
authors.affiliation: Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea 138-600. cmlim@amc.seoul.kr
authors.forename: Chae-Man
authors.initials: CM
authors.lastname: Lim
authors.forename: Myung Sun
authors.initials: MS
authors.lastname: Kim
authors.forename: Jong-Joon
authors.initials: JJ
authors.lastname: Ahn
authors.forename: Mee-Jung
authors.initials: MJ
authors.lastname: Kim
authors.forename: Youngmee
authors.initials: Y
authors.lastname: Kwon
authors.forename: Inchul
authors.initials: I
authors.lastname: Lee
authors.forename: Younsuck
authors.initials: Y
authors.lastname: Koh
authors.forename: Dong-Soon
authors.initials: DS
authors.lastname: Kim
authors.forename: Won-Dong
authors.initials: WD
authors.lastname: Kim
mesh_terms: D000208:Acute Disease; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002452:Cell Count; D007036:Hypothermia, Induced; D007375:Interleukin-1 / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000633:toxicity; D008168:Lung / Q000473:pathology*; D008297:Male; D009504:Neutrophils / Q000276:immunology*; D009195:Peroxidase / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase