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‐α, MCP‐1, superoxide and hydrogen peroxide was measured. Results: Leakage index of human serum albumin showed a significant increase early (1 h) after induction of AP and later (9 h) 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 6 h 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‐α increased significantly at 6 and 9 h in both models. Conclusion: 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.

• Abdominal sepsis
• acute pancreatitis
• endothelial barrier
• inflammatory response
• macrophages