title: Pulmonary apoptosis after supraceliac aorta clamping in a rat model.
abstract: BACKGROUND
  Lungs are a major target in several models of systemic inflammation. We investigated the effect of gut ischemia reperfusion on lung injury as apoptotic histological changes and pulmonary dysfunction.
  
  
  METHODS
  Sixteen Wistar male rats were randomized in two equal groups: a control group and a gut ischemia-reperfusion (IR) group for which gut IR was performed by clamping the supraceliac aorta during 40 min. After 60 min of reperfusion, blood gas, bronchoalveolar liquid (BAL) and pulmonary tissue were sampled for measurements. Acidosis status was used to assess the importance of gut IR. Tumor necrosis factor-alpha in the BAL reflected the inflammatory pulmonary response. A terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling method was used to quantify the percentage of apoptotic cells in BAL and to visualize apoptotic cells on tissue samples. Pulmonary dysfunction was assessed by PaO(2) measure.
  
  
  RESULTS
  Gut IR caused an important metabolic acidosis (pH = 7.19 +/- 0.05 versus 7.32 +/- 0.02, P = 0.032 and HCO(3-) = 10.8 +/- 2.54 versus 21.1 +/- 1.72 mmol/L, P = 0.027). At the pulmonary level, there was yet no hypoxemia (paO(2) = 18.1 +/- 1.85 versus 12.3 +/- 1.1 kPa, P = 0.005) but a significant inflammatory response (tumor necrosis factor-alpha in BAL = 7.5 +/- 5 versus 0 pg/mL). The number of apoptotic cell in BAL more than doubled in the gut IR group (51.3 +/- 8 versus 23 +/- 4.3%, P = 0.046). Apoptose involved pneumocytes and bronchiolar epithelial cells.
  
  
  CONCLUSIONS
  Our rat models of gut IR induced a significant pulmonary injury characterized by a doubling in apoptotic cells but not yet by a functional pulmonary impairment.
authors.affiliation: Département d'Anesthésie et de Réanimation, Hôpitaux Universitaires de Rouen, Rouen, France.
authors.forename: Olivier
authors.initials: O
authors.lastname: Collange
authors.forename: Tamion
authors.initials: T
authors.lastname: Fabienne
authors.forename: Rives
authors.initials: R
authors.lastname: Nathalie
authors.forename: Thuillez
authors.initials: T
authors.lastname: Christian
authors.forename: Richard
authors.initials: R
authors.lastname: Vincent
authors.forename: Dureuil
authors.initials: D
authors.lastname: Bertrand
authors.forename: Plissonnier
authors.initials: P
authors.lastname: Didier
mesh_terms: D000138:Acidosis / Q000209:etiology / Q000473:pathology; D000818:Animals; D001012:Aorta, Abdominal; D017209:Apoptosis; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002445:Celiac Artery; D007410:Intestinal Diseases / Q000150:complications / Q000473:pathology*; D007422:Intestines / Q000098:blood supply / Q000473:pathology; D007511:Ischemia / Q000150:complications / Q000473:pathology*; D008171:Lung Diseases / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D008297:Male; D009102:Multiple Organ Failure / Q000276:immunology / Q000473:pathology*; D011659:Pulmonary Gas Exchange; D051381:Rats; D017208:Rats, Wistar; D020545:Respiratory Mucosa / Q000276:immunology / Q000473:pathology; D013525:Surgical Instruments; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D014409:Tumor Necrosis Factor-alpha