title: Portal vein cytokines in the early phase of acute experimental oedematous and necrotizing porcine pancreatitis.
abstract: OBJECTIVE
  Cytokines initiate and modify systemic inflammatory response in early acute pancreatitis. The aim of this study was to analyze which cytokines are released from the pancreas to portal venous blood in the early phase of acute experimental necrotizing and oedematous pancreatitis and which of those cytokines are correlated with the more severe form of the disease.
  
  
  METHODS
  Fifteen pigs were randomized to develop mild oedematous pancreatitis (n = 5, saline infusion to pancreatic duct), severe necrotizing pancreatitis (n = 5, taurocholic acid infusion) along with a control group (n = 5). Arterial and venous blood samples were drawn and cytokine levels were measured from portal vein blood at 0, 120, 240 and 360 min after the induction of pancreatitis. Tissue samples from the pancreas were harvested at 0 and 360 min.
  
  
  RESULTS
  White blood cell count increased in necrotizing pancreatitis and the control group. The amount of neutrophils increased (p < 0.001) and the lymphocyte and eosinophil counts decreased in all groups (p < 0.001, p < 0.001). The monocyte count, as well as PDGF and IL-6 concentrations, increased only in necrotizing pancreatitis. IL-8 and eotaxin increased both in oedematous and necrotizing pancreatitis. MCP-1 increased in all groups. IL-9, IL-4, MIP-1α, IFN- γ concentrations did not change. Eotaxin and MCP-1 plasma levels from a previous series between portal venous and pulmonary arterial blood were not significantly different.
  
  
  CONCLUSIONS
  The initial inflammatory process was diverse in oedematous and necrotizing pancreatitis. Increased monocyte count in combination with elevated PDGF and IL-6 are characteristic of necrotizing pancreatitis in our model.
authors.affiliation: Department of Surgery, Oulu University Hospital, Oulu, Finland. sanna.merilainen@mail.suomi.net
authors.forename: Sanna
authors.initials: S
authors.lastname: Meriläinen
authors.forename: Jyrki
authors.initials: J
authors.lastname: Mäkelä
authors.forename: Hanna Alaoja
authors.initials: HA
authors.lastname: Jensen
authors.forename: Sebastian
authors.initials: S
authors.lastname: Dahlbacka
authors.forename: Siri
authors.initials: S
authors.lastname: Lehtonen
authors.forename: Toni
authors.initials: T
authors.lastname: Karhu
authors.forename: Karl-Heinz
authors.initials: KH
authors.lastname: Herzig
authors.forename: Meeri
authors.initials: M
authors.lastname: Kröger
authors.forename: Vesa
authors.initials: V
authors.lastname: Koivukangas
authors.forename: Juha
authors.initials: J
authors.lastname: Koskenkari
authors.forename: Pasi
authors.initials: P
authors.lastname: Ohtonen
authors.forename: Tuomo
authors.initials: T
authors.lastname: Karttunen
authors.forename: Petri
authors.initials: P
authors.lastname: Lehenkari
authors.forename: Tatu
authors.initials: T
authors.lastname: Juvonen
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D016207:Cytokines / Q000097:blood*; D004195:Disease Models, Animal; D004487:Edema / Q000097:blood* / Q000139:chemically induced / Q000150:complications; D004804:Eosinophils; D007958:Leukocyte Count; D018655:Lymphocyte Count; D009000:Monocytes; D009504:Neutrophils; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood* / Q000139:chemically induced / Q000150:complications; D010982:Platelet-Derived Growth Factor / Q000378:metabolism; D011169:Portal Vein; D011651:Pulmonary Artery; D012965:Sodium Chloride; D013552:Swine; D013656:Taurocholic Acid; D013997:Time Factors
chemical_list: D016207:Cytokines; D010982:Platelet-Derived Growth Factor; D012965:Sodium Chloride; D013656:Taurocholic Acid