title: Exogenous and endogenous nitric oxide donors improve post-ischemic tissue oxygenation in early pancreatic ischemia/reperfusion injury in the rat.
abstract: BACKGROUND
  In pancreatic ischemia/reperfusion (IR) injury (IRI) the role of nitric oxide (NO) is not completely understood. Using a rat model of normothermic in situ IRI, the effect of endogenous and exogenous NO donors on post-ischemic tissue oxygenation and tissue damage was investigated.
  
  
  METHODS
  IR was induced by 2-hour normothermic in situ ischemia of a pancreatic tail segment pedunculated on the splenic vessels with 2 h of reperfusion in an untreated, an L-arginine- and a sodium-nitroprusside-treated group (Wistar rats, n = 7/group). Animals without ischemia served as controls. Tissue oxygenation (pO(2ti)) was monitored using a pO2-sensitive Clark-type electrode. Histological investigation was performed following a semiquantitative score (edema, vacuolization, PMN infiltration, necrosis). Plasma lipase was another marker of organ damage.
  
  
  RESULTS
  The administration of L-arginine and sodium nitroprusside caused a significant amelioration of the decrease in pO2i) after reperfusion compared to IR animals (p < 0.05). Histological damage was also reduced in the NO donor groups (p < 0.05). After reperfusion, plasma lipase in the L-arginine-treated animals was significantly lower compared to IR and sodium nitroprusside (p < 0.05).
  
  
  CONCLUSIONS
  The administration of both endogenous and exogenous NO donors is protective in IRI of the rat pancreas which can be seen by an improvement in post-ischemic tissue oxygenation which indicates better nutritive tissue perfusion, amelioration of the histological tissue injury and, in L-arginine animals, lower lipase levels. NO donors could be useful in the prevention and reduction of the pancreatic IRI.
authors.affiliation: Department of Surgery, University of Freiburg, Freiburg, Germany. obermai@ch11.ukl.uni-freibrug.de
authors.forename: R
authors.initials: R
authors.lastname: Obermaier
authors.forename: E
authors.initials: E
authors.lastname: Von Dobschuetz
authors.forename: A
authors.initials: A
authors.lastname: Benthues
authors.forename: N
authors.initials: N
authors.lastname: Ansorge
authors.forename: W
authors.initials: W
authors.lastname: Schareck
authors.forename: U T
authors.initials: UT
authors.lastname: Hopt
authors.forename: S
authors.initials: S
authors.lastname: Benz
mesh_terms: D000818:Animals; D001794:Blood Pressure; D008049:Lipase / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000378:metabolism / Q000494:pharmacology*; D010100:Oxygen / Q000378:metabolism; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology
chemical_list: D020030:Nitric Oxide Donors; D009569:Nitric Oxide; D008049:Lipase; D010100:Oxygen