Abstract
Abstract Objective: To investigate the role of acute inflammation of the peritoneal cavity in adhesion formation. Design: Prospective randomized, controlled trial Setting: University laboratory research centerAnimals: 9-10 weeks old BALB/c female mice Interventions: In our laparoscopic mouse model acute inflammation of the peritoneal cavity and adhesion formation were evaluated in a control group with CO2 pneumoperitoneum (PP)-enhanced adhesions, in CO2 PP plus manipulation-enhanced adhesions and in the latter group + dexamethasone-reduced adhesions. Adhesions and acute inflammation were assessed by neoangiogenesis, diapedesis and leukocytes accumulation on the 2nd day after surgery. Main outcome measure(s): Qualitative and quantitative adhesion scores and an acute inflammation score.Results: Adhesions were enhanced by the CO2 PP (p=0.007), further enhanced by manipulation (p<0.0001 versus CO2 PP) and decreased by the administration of dexamethasone (p<0.0001 versus CO2 PP+manipulation ). Acute inflammation scores strongly correlated with total adhesion score whether assessed as total inflammation score (p<0.0001) or as neoangiogenesis (p<0.0002), diapedesis (p<0.03) or leukocyte accumulation (p<0.0002). Inflammation scores, moreover, were strikingly similar at the surgical lesion and at the parietal peritoneum. Conclusions: These data strongly suggest that acute inflammation in the entire peritoneum cavity is the driving mechanism of adhesion formation at the lesion site.
Highlights
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Summary
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