title: Acute edematous and necrotic pancreatitis in a porcine model.
abstract: OBJECTIVE
  It is unclear why pancreatitis progresses either to mild edematous disease or to severe necrotic disease. The aim of the study was to shed some light on this topic by investigating differences during the early stages of necrotic and edematous pancreatitis.
  
  
  METHODS
  Piglets were randomized into two groups. Necrotic pancreatitis was induced with retrograde injection of 20% taurocholic acid (1 ml/kg), and edematous pancreatitis was induced with 0.9% NaCl (1 ml/kg). Central hemodynamics was measured, and pancreatic microcirculation was directly examined by intravital microscopy. Vascular permeability to proteins and albumin was measured by microdialysis. Apoptosis and claudins 2, 3, 4, 5, and 7 were analyzed from pancreatic tissue samples. Blood samples were taken for analysis of blood cell counts, blood gases, lipase, and amylase.
  
  
  RESULTS
  Hemodynamic changes were similar in both groups, whereas microcirculatory impairment was more pronounced in necrotic pancreatitis. Necrosis was associated only with necrotic pancreatitis. Apoptosis increased only in edematous pancreatitis. The number of blood neutrophils and monocytes increased and lymphocyte and platelet counts decreased in both groups. Necrotic pancreatitis was associated with increased permeability to albumin and proteins. Expression of claudins 3, 4, 5, and 7 was not changed during pacreatitis, but in acinar cells, membranous expression of claudin-2 increased in both groups.
  
  
  CONCLUSIONS
  The results show that acute edematous pancreatitis is characterized by induction of apoptosis, whereas full-blown pancreatitis is characterized by necrosis. Impaired vascular permeability to albumin and protein is related to the early phase of necrotic pancreatitis. Claudin-2 increases during acute necrotic and edematous pancreatitis and may be related to impaired permeability.
authors.affiliation: Department of Surgery, Oulu University Hospital, University of Oulu, Oulu, Finland. memerila@paju.oulu.fi
authors.forename: Sanna
authors.initials: S
authors.lastname: Meriläinen
authors.forename: Jyrki
authors.initials: J
authors.lastname: Mäkelä
authors.forename: Vesa
authors.initials: V
authors.lastname: Anttila
authors.forename: Vesa
authors.initials: V
authors.lastname: Koivukangas
authors.forename: Hanna
authors.initials: H
authors.lastname: Kaakinen
authors.forename: Eija
authors.initials: E
authors.lastname: Niemelä
authors.forename: Pasi
authors.initials: P
authors.lastname: Ohtonen
authors.forename: Juha
authors.initials: J
authors.lastname: Risteli
authors.forename: Tuomo
authors.initials: T
authors.lastname: Karttunen
authors.forename: Ylermi
authors.initials: Y
authors.lastname: Soini
authors.forename: Tatu
authors.initials: T
authors.lastname: Juvonen
mesh_terms: D000818:Animals; D002199:Capillary Permeability; D004195:Disease Models, Animal; D004487:Edema / Q000209:etiology*; D008833:Microcirculation; D010179:Pancreas / Q000098:blood supply*; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D012720:Severity of Illness Index; D013552:Swine