title: The nitric oxide donor sodium nitroprusside is protective in ischemia/reperfusion injury of the pancreas.
abstract: BACKGROUND
  The role of nitric oxide in the ischemia/reperfusion injury of the pancreas is still unclear. In other organs, protective as well as aggravating effects have been described. We have, therefore, investigated the effect of the nitric oxide donor sodium nitroprusside on pancreatic ischemia/reperfusion injury.
  
  
  METHODS
  In Landrace pigs, after transsection of the pancreas, complete vascular isolation of the pancreatic tail was performed. The tail was subjected to 3 hr of warm ischemia and thereafter reperfusion (6 hr). The animals were divided into a control group (n=7) and a treatment group (n=7) that received 15 mg of sodium nitroprusside after reperfusion intra-arterially into the splenic artery.
  
  
  RESULTS
  The morphological tissue damage and lipase activity in the venous effluent of the pancreas were significantly lower in the treatment group. Partial oxygen tension in the tissue after reperfusion was markedly reduced in the control group, indicating an impairment of microcirculation. In the treatment group, however, partial oxygen tension in the tissue was significantly higher (43 vs. 20 mmHg; P<0.014). Furthermore, total blood flow through the pancreatic tail in the treatment group was found to be significantly higher in the late reperfusion period (14 vs. 9.5 ml/min at 5 hr after reperfusion; P<0.05).
  
  
  CONCLUSIONS
  There is a marked impairment of pancreatic microcirculation after reperfusion. Sodium nitroprusside counteracts this impairment and has a protective effect on ischemia/reperfusion injury of the pancreas.
authors.affiliation: Department of Surgery, University of Rostock, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Benz
authors.forename: R
authors.initials: R
authors.lastname: Schnabel
authors.forename: H
authors.initials: H
authors.lastname: Weber
authors.forename: F
authors.initials: F
authors.lastname: Pfeffer
authors.forename: R
authors.initials: R
authors.lastname: Wiesner
authors.forename: P
authors.initials: P
authors.lastname: von Breitenbuch
authors.forename: H
authors.initials: H
authors.lastname: Nizze
authors.forename: W
authors.initials: W
authors.lastname: Schareck
authors.forename: U T
authors.initials: UT
authors.lastname: Hopt
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D005260:Female; D005978:Glutathione / Q000378:metabolism; D007511:Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D020030:Nitric Oxide Donors / Q000627:therapeutic use*; D009599:Nitroprusside / Q000627:therapeutic use*; D010100:Oxygen / Q000378:metabolism; D010179:Pancreas / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D010313:Partial Pressure; D011453:Prostaglandins / Q000097:blood; D012039:Regional Blood Flow / Q000187:drug effects; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013552:Swine; D014357:Trypsin / Q000097:blood
chemical_list: D020030:Nitric Oxide Donors; D011453:Prostaglandins; D009599:Nitroprusside; D000255:Adenosine Triphosphate; D014357:Trypsin; D005978:Glutathione; D010100:Oxygen