title: Mild hypothermia reduces expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of neutrophils after acid-induced lung injury in the rat.
abstract: BACKGROUND
  The pathophysiology of the acute phase of acid-induced lung injury (AILI) has been elucidated. However, once acute respiratory distress syndrome (ARDS) develops, the mortality rate remains high and there is, as yet, no effective therapy. There are reports that application of mild hypothermia is an effective treatment for ARDS. In this study, we hypothesize that mild hypothermia inhibits activation of neutrophils and expression of intercellular adhesion molecule-1 (ICAM-1) in an injured lung. We studied the effects of mild hypothermia on the expression of ICAM-1 and the accumulation of neutrophils after AILI in the rat.
  
  
  METHODS
  Male Sprague-Dawley rats were randomly allocated to one of the four groups: control normothermic group, induced mild hypothermia group, acid-instilled normothermic group, and acid-instilled group with mild hypothermia. At 6 h after instillation of acid, lungs were removed to measure neutrophil activity and to detect the expression of ICAM-1 in each group.
  
  
  RESULTS
  Oxygenation in acid-instilled rats was significantly impaired as compared to that in non-instilled groups, but induction of mild hypothermia gradually improved oxygenation. Expression of ICAM-1 was enhanced in the acid-instilled normothermic group. By contrast, no overexpression of ICAM-1 and its mRNA was detected in the acid-instilled hypothermic group. In addition, accumulation of neutrophils was markedly inhibited after exposure to mild hypothermia irrespective of the instillation of acid.
  
  
  CONCLUSIONS
  Our data suggest mild hypothermia can inhibit the adhesion, activation, and accumulation of neutrophils during the acute phase of AILI in the rat and may have the potential to reduce ongoing inflammation of ALI or ARDS.
authors.affiliation: 1st Department of Pathology, Oita University Faculty of Medicine, Hasama-machi, Oita, Japan. kira@med.oita-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Kira
authors.forename: T
authors.initials: T
authors.lastname: Daa
authors.forename: K
authors.initials: K
authors.lastname: Kashima
authors.forename: M
authors.initials: M
authors.lastname: Mori
authors.forename: T
authors.initials: T
authors.lastname: Noguchi
authors.forename: S
authors.initials: S
authors.lastname: Yokoyama
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western / Q000379:methods; D004195:Disease Models, Animal; D007036:Hypothermia, Induced / Q000379:methods*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*; D008297:Male; D009504:Neutrophils / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D009195:Peroxidase / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000139:chemically induced* / Q000473:pathology / Q000628:therapy*; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods
chemical_list: D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase; D010100:Oxygen