title: Effects of octreotide in acute hemorrhagic necrotizing pancreatitis in rats.
abstract: OBJECTIVE
  Octreotide is considered to reduce exocrine pancreatic secretion in acute hemorrhagic necrotizing pancreatitis decreasing pancreatic autodigestion. The aim of this study was to determine whether octreotide also has antioxidative effects in acute pancreatitis. Additionally time and dose of application were of interest.
  
  
  METHODS
  Ninety male Sprague-Dawley rats were randomized into six groups (n = 15). Group 1 underwent a laparotomy, and animals in groups 2-6 received intraductal glycodeoxycholic acid followed by intravenous cerulein. Groups 3 and 4 were injected with 0.5 mg octreotide, while groups 5 and 6 received continuous intravenous infusion of 0.05 mg octreotide/h for 10 h. Treatment was initiated 6 hours after induction of pancreatitis (IP) in groups 3 and 5, and 14 h after IP in groups 4 and 6. At 24 h after IP all animals were killed and each pancreas was analyzed histopathologically. In addition, levels of pancreatic lipid peroxidation protective enzymes glutathione-peroxidase (GSH-Px) and superoxide dismutase (SOD) as well as lipid peroxidation via thiobarbituric acid reactive substances (TBARS) were determined.
  
  
  RESULTS
  Early bolus application of octreotide reduced severity of histopathological changes in acute pancreatitis and decreased lipid peroxidation in pancreatic tissue samples; however, late bolus application and continuous intravenous infusion did not influence pancreatitis or lipid peroxidation.
  
  
  CONCLUSIONS
  Octreotide seems to have a dose- and time-dependent effect on histopathology and lipid peroxidation in a model of pancreatitis in rats.
authors.affiliation: Clinic of Surgery and Center of Minimal-Invasive Surgery, Kliniken Essen-Mitte, Essen, Germany. charipanc@aol.com
authors.forename: Frank Axel
authors.initials: FA
authors.lastname: Wenger
authors.forename: Maik
authors.initials: M
authors.lastname: Kilian
authors.forename: Ina
authors.initials: I
authors.lastname: Heukamp
authors.forename: Thomas
authors.initials: T
authors.lastname: Foitzik
authors.forename: Christoph Andreas
authors.initials: CA
authors.lastname: Jacobi
authors.forename: Hans
authors.initials: H
authors.lastname: Guski
authors.forename: Ingolf
authors.initials: I
authors.lastname: Schimke
authors.forename: Joachim Michael
authors.initials: JM
authors.lastname: Müller
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D002108:Ceruletide; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005979:Glutathione Peroxidase / Q000378:metabolism; D006002:Glycodeoxycholic Acid; D006470:Hemorrhage / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007262:Infusions, Intravenous; D007275:Injections, Intravenous; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D015282:Octreotide / Q000008:administration & dosage / Q000494:pharmacology*; D010179:Pancreas / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D006002:Glycodeoxycholic Acid; D002108:Ceruletide; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D015282:Octreotide