title: Exhaled carbon monoxide and inducible heme oxygenase expression in a rat model of postperfusion acute lung injury.
abstract: OBJECTIVE
  Expression of inducible heme oxygenase has been shown to be increased in various visceral inflammatory disorders, which may confer a protective role. The purpose of our study was to determine whether the expression of inducible heme oxygenase was up-regulated within lungs in a rat model of extracorporeal circulation.
  
  
  METHODS
  Wistar rats underwent either a partial femoro-femoral extracorporeal circulation in normothermia for 3 hours (n = 5) or a sham procedure (n = 5). Exhaled carbon monoxide concentration was monitored with an infrared analyzer. After the rats were killed, lungs were harvested for determination of heme oxygenase activity and inducible heme oxygenase expression (by Western blot and immunohistochemistry). Lung injury was also assessed by arterial blood gas analysis and microscopic study.
  
  
  RESULTS
  Extracorporeal circulation was responsible for a lung injury characterized by decreased arterial blood oxygen saturation and typical morphologic findings (marked alveolar neutrophil infiltration; interstitial edema). Exhaled carbon monoxide concentration remained stable throughout the experiment in all sham rats, whereas it increased after extracorporeal circulation (from 0.16 +/- 0.05 ppm at baseline to 0.7 +/- 0.2 ppm at end of experiment; P =.0001). Pulmonary heme oxygenase activity and inducible heme oxygenase content (assessed by Western blot) were increased within lungs of rats that underwent extracorporeal circulation. Immunohistochemistry revealed that the expression of inducible heme oxygenase was mainly localized to inflammatory cells.
  
  
  CONCLUSIONS
  Post-extracorporeal circulation acute lung injury in rats was associated with an increased expression of inducible heme oxygenase, the functional significance of which remains to be determined.
authors.affiliation: Laboratoire d'Etudes des Greffes et Prothèses Cardiaques, Hôpital Broussais, Paris, France. rzegdi@hotmail.com
authors.forename: Rachid
authors.initials: R
authors.lastname: Zegdi
authors.forename: Olivier
authors.initials: O
authors.lastname: Fabre
authors.forename: Nermine
authors.initials: N
authors.lastname: Lila
authors.forename: Paul
authors.initials: P
authors.lastname: Fornès
authors.forename: Michèle
authors.initials: M
authors.lastname: Cambillau
authors.forename: Ming
authors.initials: M
authors.lastname: Shen
authors.forename: Philippe
authors.initials: P
authors.lastname: Hervé
authors.forename: Alain
authors.initials: A
authors.lastname: Carpentier
authors.forename: Jean-Noël
authors.initials: JN
authors.lastname: Fabiani
mesh_terms: D000208:Acute Disease; D000818:Animals; D015153:Blotting, Western; D001944:Breath Tests; D002248:Carbon Monoxide / Q000032:analysis*; D005112:Extracorporeal Circulation; D006419:Heme Oxygenase (Decyclizing) / Q000096:biosynthesis*; D051547:Heme Oxygenase-1; D007150:Immunohistochemistry; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism*; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D015854:Up-Regulation
chemical_list: D002248:Carbon Monoxide; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1