title: The effects of somatostatin on the microperfusion of the pancreas during acute necrotizing pancreatitis in rats.
abstract: OBJECTIVE
  Autodigestion and impairment of microcirculation of the pancreas play an important role in the pathogenesis of acute pancreatitis. Somatostatin with the reducing effect on the hepato-splanchnic blood flow decreases exocrine pancreatic secretion. Microcirculatory changes are central to the pathogenesis of acute pancreatitis. However, little is known about the effects of somatostatin on the pancreatic tissue oxygen pressure and acinar cell injury during acute pancreatitis. The aim was to evaluate somatostatin by measuring its effect on the pancreatic tissue oxygen pressure and acinar injury in acute pancreatitis.
  
  
  METHODS
  Acute necrotizing pancreatitis was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptide was measured to verify comparable disease severity. After the induction of acute necrotizing pancreatitis, animals randomly received either ringer lactate or somatostatin. Monitoring included cardiorespiratory parameters, hematocrit, amylase, pancreatic tissue oxygen pressure, and trypsinogen activation peptide levels. At the end of the experiments the pancreas was removed for evaluation of acinar cell injury.
  
  
  RESULTS
  The two study groups were comparable with regard to mean arterial pressure, heart rate, arterial blood gases, hematocrit, and serum amylase. The induction of pancreatitis resulted in the significant decrease of pancreatic tissue oxygen pressure in both groups. The use of somatostatin did not increase pancreatic tissue oxygen pressure. There were no significant differences in plasma trypsinogen activation peptide and serum amylase levels in the animals of two treatment groups. Only somatostatin decreased pancreatic damage significantly.
  
  
  CONCLUSIONS
  The use of somatostatin did not improve pancreatic microcirculation or trypsinogen activation peptide level in acute necrotizing pancreatitis; however, it reduced pancreatic damage. Therefore, it has a limited value in the treatment of the acute pancreatitis.
authors.affiliation: Department of Surgery, Karadeniz Technical University, Trabzon, Turkey.
authors.forename: Metin
authors.initials: M
authors.lastname: Piri
authors.forename: Etem
authors.initials: E
authors.lastname: Alhan
authors.forename: Uzer
authors.initials: U
authors.lastname: Küçüktülü
authors.forename: Cengiz
authors.initials: C
authors.lastname: Erçin
authors.forename: Orhan
authors.initials: O
authors.lastname: Deger
authors.forename: Kadir
authors.initials: K
authors.lastname: Yücel
authors.forename: Ramazan
authors.initials: R
authors.lastname: Cicek
mesh_terms: D000818:Animals; D006728:Hormones / Q000494:pharmacology*; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009842:Oligopeptides / Q000097:blood; D010100:Oxygen / Q000378:metabolism; D010179:Pancreas / Q000098:blood supply* / Q000187:drug effects; D019283:Pancreatitis, Acute Necrotizing / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013004:Somatostatin / Q000494:pharmacology*
chemical_list: D006728:Hormones; D009842:Oligopeptides; C080396:trypsinogen activation peptide; D013004:Somatostatin; D010100:Oxygen