title: N-acetyl cysteine improves glycogenesis after segmental liver ischemia and reperfusion injury in pigs.
abstract: OBJECTIVE
  N-acetylcysteine (NAC) is an antioxidative molecule known to protect liver tissue from oxygen radical species generated during ischemia and reperfusion (IR). Nutritional and toxicology studies have shown that NAC also improves glucose metabolism and glycogen stores. We hypothesized that NAC improves glycogenesis and that impaired glycogenesis is a key element in IR injury.
  
  
  METHODS
  In an experimental model, 80 min of segmental liver ischemia was induced in 16 pigs and the reperfusion was followed for 360 min. Eight animals received NAC 150 mg/kg as a bolus injection followed by an infusion of NAC 50 mg/kg/h intravenously.
  
  
  RESULTS
  AST and leukocyte density were lower in the NAC-treated animals, unrelated to the glutathione levels or apoptosis. Glycogen stores returned to a higher degree in the NAC-treated animals and microdialysis revealed lower levels of lactate during the reperfusion phase. Nitrite/Nitrate levels in the NAC group were lower in both serum and microdialysates, indicating that NAC scavenges radical nitrosative species.
  
  
  CONCLUSIONS
  NAC treatment improves glycogenesis after liver IR injury and reduces the level of intraparenchymal lactate during reperfusion, possibly due to the scavenging of radical nitrosative species.
authors.affiliation: Division of Surgery, University Hospital, Linköping, Sweden. anders.winbladh@lio.se
authors.forename: Anders
authors.initials: A
authors.lastname: Winbladh
authors.forename: Bergthor
authors.initials: B
authors.lastname: Björnsson
authors.forename: Lena
authors.initials: L
authors.lastname: Trulsson
authors.forename: Linda
authors.initials: L
authors.lastname: Bojmar
authors.forename: Tommy
authors.initials: T
authors.lastname: Sundqvist
authors.forename: Per
authors.initials: P
authors.lastname: Gullstrand
authors.forename: Per
authors.initials: P
authors.lastname: Sandström
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis; D001219:Aspartate Aminotransferases / Q000097:blood; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D006003:Glycogen / Q000096:biosynthesis*; D019344:Lactic Acid / Q000378:metabolism; D007958:Leukocyte Count; D008099:Liver / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D017551:Microdialysis; D009504:Neutrophils; D009566:Nitrates / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013552:Swine
chemical_list: D016166:Free Radical Scavengers; D009566:Nitrates; D009573:Nitrites; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D006003:Glycogen; D001219:Aspartate Aminotransferases; D005978:Glutathione; D000111:Acetylcysteine