Mechanisms of multiple organ damages in acute necrotizing pancreatitis

Abstract

Objective: To determine the role of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), and evaluate the progress from SIRS to MODS and the therapeutic strategies for acute necrotizing pancreatitis (ANP).

Methods: Rat ANP models were made by retrograde injection of 3.5% sodium taurocholate 2.5 ml/kg into the pancreatic duct. Serum interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF alpha), amylase, endotoxin, and albumin were examined. The morphology and pathology of the pancreas, liver, lung, kidney and heart after ANP were observed. Finally, TNF alpha mRNA in the liver, lung, kidney and heart after ANP were observed by reverse transcriptase-polymerase chain reactions, and the efficiency of somatostatin and growth hormone were also observed in this experiment.

Results: ANP led to remarkable elevation of the inflammatory mediators which were positively correlated with the development of ANP and MODS. Somatostatin and growth hormone inhibited inflammatory mediators and TNF alpha mRNA overexpressions, reduced the risk of MODS, corrected hypoalbuminemia, reversed negative nitrogen balance, and controlled the reduction of cell groups with functions and reasonably intervened SIRS caused by ANP.

Conclusion: TNF alpha mRNA plays an important role in ANP progression. The amelioration of ANP by combination treatment with somatostatin and growth hormone leads to the reduction of complications and marked increase in survival.