title: Does the septic shock interfere experimental acute pancreatitis in rats?
abstract: BACKGROUND
  Acute pancreatitis is a disease involving pro-inflammatory mediators. Two complex and multifactorial pathogenetic ways lead to edematous or necrotizing pancreatitis. The course of the disease is thought to be the consequence of an acute inflammatory response.
  
  
  OBJECTIVE
  The authors examined the impact of Escherichia coli LPS on the acute cerulein pancreatitis in rats.
  
  
  METHODS
  The study was performed on rats using the ceruleine pancreatitis model. The activation status of polymorphonuclear cells, blood IL-6 concentration, oxidative stress parameters, pancreatic enzymes concentration and microscopic alterations were determined at 5th and 9th h observations.
  
  
  RESULTS
  In acute pancreatitis and acute pancreatitis with LPS groups, the peripheral polymorphonuclear cells activity was lower than in control one. Authors noticed the same neutrophil activation in acute pancreatitis after lipopolysaccharide administration although the peripheral blood polymorphonuclear cells count was significantly higher at the 9th h observation. LPS neither changed the oxidative stress within pancreatic gland, nor amylase or serum lipase activity. LPS given to acute pancreatitis animals resulted in significant increase of serum IL-6 concentration at 5th observation turning normal after 9th h.
  
  
  CONCLUSIONS
  Collected data supports thesis of early polymorphonuclear cells involvement in acute pancreatitis and oxidative stress evidence in pancreatic parenchyma. However, results did not reveal that administration of LPS amplified inflammatory response during the course of acute pancreatitis.
authors.affiliation: Department of General Endocrine & Transplant Surgery, Medical University of Gdansk, 7 Debinki Street, 80-952 Gdansk, Poland. sthac@amg.gda.pl
authors.forename: S
authors.initials: S
authors.lastname: Hac
authors.forename: M
authors.initials: M
authors.lastname: Dobosz
authors.forename: J J
authors.initials: JJ
authors.lastname: Kaczor
authors.forename: S
authors.initials: S
authors.lastname: Dobrowolski
authors.forename: J
authors.initials: J
authors.lastname: Krajewski
authors.forename: R
authors.initials: R
authors.lastname: Rzepko
authors.forename: Z
authors.initials: Z
authors.lastname: Gruca
authors.forename: Z
authors.initials: Z
authors.lastname: Sledzinski
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D002108:Ceruletide; D004195:Disease Models, Animal; D015850:Interleukin-6 / Q000097:blood; D007958:Leukocyte Count; D008049:Lipase / Q000097:blood; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D018375:Neutrophil Activation; D009504:Neutrophils / Q000166:cytology; D018384:Oxidative Stress; D010179:Pancreas / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000097:blood / Q000276:immunology* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012772:Shock, Septic / Q000097:blood / Q000139:chemically induced / Q000276:immunology*
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D002108:Ceruletide; D008049:Lipase; D000681:Amylases