title: [Protective effect of nitric oxide on pancreas and its relation to sulfhydryl compounds and oxygen free radicals].
abstract: OBJECTIVE
  To investigate the effect of endogenous nitric oxide (NO) on acute necrosis pancreatitis in rats and its relation to sulfhydryl compounds and lipid peroxidation.
  
  
  METHODS
  Acute necrosis pancreatitis in rats was induced by retrograde sodium taurocholate (5%) infusion into the pancreatobiliary duct (1 ml/kg body weight), and N(G)-nitro-L-arginine (L-NNA) was used as the inhibitor of endogenous NO. The effect of endogenous NO on pancreatic injury, serum amylase level, the pancreatic tissue levels of sulfhydryl compounds, and malonaldehyde (MDA, the end product of lipid peroxidation) was evaluated, respectively.
  
  
  RESULTS
  Sodium taurocholate administration induced evident pancreatic tissue edema and acinar necrosis, and intrapancreatic hemorrhage occurred in 2/7 rats. Both serum amylase and tissue MDA [(1.25 +/- 0.28) nmol/mg x pr vs. (0.5 +/- 0.03) nmol/mg x pr, P < 0.05] were significantly increased, but tissue sulfhydryl compounds were decreased markedly. Pretreatment with the NO inhibitor, L-NNA (12.5 mg/kg body weight), significantly intensified acinar necrosis and increased the intrapancreatic hemorrhage (10/12). L-NNA also resulted in a further increase of serum amylase and tissue MDA [(3.0 +/- 0.40) vs. (1.25 +/- 0.28) nmol/mg x pr, P < 0.05], but it had no effect on the tissue sulfhydryl compounds.
  
  
  CONCLUSIONS
  Endogenous NO has the effect of pancreatic protection, and its antioxidation may be responsible, at least in part, for the protective mechanisms. Sulfhydryl compounds may not be involved in NO's pancreatic protection mechanisms.
authors.affiliation: Department of Surgery, Xuanwu Hospital, Capital Medical Science University, Beijing 100053, China.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.forename: J
authors.initials: J
authors.lastname: Sun
authors.forename: F
authors.initials: F
authors.lastname: Li
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Cui
authors.forename: H
authors.initials: H
authors.lastname: Sun
authors.forename: S
authors.initials: S
authors.lastname: Liu
mesh_terms: D000681:Amylases / Q000097:blood; D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009569:Nitric Oxide / Q000502:physiology*; D019335:Nitroarginine / Q000008:administration & dosage; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism*; D013656:Taurocholic Acid / Q000633:toxicity*
chemical_list: D013438:Sulfhydryl Compounds; D019335:Nitroarginine; D009569:Nitric Oxide; D008315:Malondialdehyde; D013656:Taurocholic Acid; D000681:Amylases