title: Acute phase response in acute pancreatitis: a comparison with abdominal sepsis.
abstract: BACKGROUND
  Increased knowledge on the underlying pathophysiological mechanisms in acute pancreatitis (AP) and abdominal sepsis (AS) is essential, not least for the development of novel ways of treatment. The present study aims at determining dynamic changes in the systemic inflammatory response in AP and AS.
  
  
  METHODS
  AP was induced by the intraductal injection of sodium taurodeoxycholate in the rat, while AS was induced by caecal ligation and puncture. The animals were killed 1, 3, 6 and 9 h after challenge. Plasma exudation of radiolabelled albumin, myeloperoxidase (MPO), TNF-alpha, MCP-1, superoxide and hydrogen peroxide was measured.
  
  
  RESULTS
  Leakage index of human serum albumin showed a significant increase early (I h) after induction of AP and later (9h) in AS compared to controls (P < 0.05). Hydrogen peroxide generation by circulating monocytes/macrophages was high early (1 h) in AP and after 3 and 6h in AS. Superoxide generation increased by time after both challenges. MPO activity increased significantly, starting at 3 h in both AP and AS (P < 0.05). TNF-alpha increased significantly at 6 and 9 h in both models.
  
  
  CONCLUSIONS
  Our results indicate differences in the release of systemic inflammatory mediators and cellular response in AP and AS. However, potential similarities in end-effect, such as the development of remote organ injury (lungs), may exist as implied by the MPO results. Further investigations of the mechanisms are crucial.
authors: Dept. of Surgery, Lund University Hospital, Lund, Sweden.
authors: M
authors: M
authors: Dib
authors: X
authors: X
authors: Zhao
authors: X
authors: X
authors: Wang
authors: E
authors: E
authors: Andersson
authors: G
authors: G
authors: Drewsen
authors: R
authors: R
authors: Andersson
mesh_terms: D000005:Abdomen; D000208:Acute Disease; D000210:Acute-Phase Reaction / Q000503:physiopathology*; D000818:Animals; D002199:Capillary Permeability; D018932:Chemokine CCL2 / Q000032:analysis; D008264:Macrophages / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000378:metabolism; D010195:Pancreatitis / Q000503:physiopathology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000503:physiopathology*; D013481:Superoxides / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D018932:Chemokine CCL2; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D009195:Peroxidase