title: Evaluation of N-acetylcysteine treatment in acute pancreatitis-induced lung injury.
abstract: OBJECTIVE
  Pulmonary complications are frequent during acute pancreatitis (AP). We investigate the effects of N-acetylcysteine (NAC) on lung injury in mild and severe AP.                                               ANIMALS AND TREATMENT:                          Mild and severe AP was induced in rats by bile-pancreatic duct obstruction (BPDO) and infusion of 3.5 % sodium taurocholate (NaTc) into the bile-pancreatic duct, respectively. NAC (50 mg/kg) was given 1 h before and 1 h after AP.
  
  
  METHODS
  Amylase activity was measured in plasma. Lungs were harvested for mRNA expression analysis of monocyte chemoattractant protein-1 (MCP-1), cytokine-induced neutrophil chemoattractant (CINC), P-selectin and intercellular adhesion molecule-1 (ICAM-1), myeloperoxidase (MPO) activity and histological examination.
  
  
  RESULTS
  Hyperamylasemia was reduced by NAC in both AP models. NAC down-regulated MCP-1, CINC and P-selectin in BPDO- but not in NaTc-induced AP. Pulmonary insults did not vary in mild AP and were exacerbated in severe AP by NAC treatment. NAC reduced lung MPO activity in mild but not in severe AP.
  
  
  CONCLUSIONS
  Although NAC treatment down-regulated inflammatory mediators in lungs during AP it did not prevent leukocyte infiltration, which could be responsible for maintaining the lung injury. As a result, NAC aggravated the lung damage in severe AP and failed to exert beneficial effects in the mild disease model.
authors.affiliation: Departamento Fisiología y Farmacología-IBSAL, University of Salamanca, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain.
authors.forename: Sara
authors.initials: S
authors.lastname: Yubero
authors.forename: Laura
authors.initials: L
authors.lastname: Ramudo
authors.forename: Manuel A
authors.initials: MA
authors.lastname: Manso
authors.forename: Francisco
authors.initials: F
authors.lastname: Collía
authors.forename: Isabel
authors.initials: I
authors.lastname: De Dios
mesh_terms: D000111:Acetylcysteine / Q000627:therapeutic use*; D000681:Amylases / Q000097:blood; D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics; D054360:Chemokine CXCL1 / Q000235:genetics; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D008168:Lung / Q000378:metabolism / Q000473:pathology; D055370:Lung Injury / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D008297:Male; D010195:Pancreatitis / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D054360:Chemokine CXCL1; C513297:Cxcl1 protein, rat; D016166:Free Radical Scavengers; D012333:RNA, Messenger; D013656:Taurocholic Acid; D009195:Peroxidase; D000681:Amylases; D000111:Acetylcysteine