Introduction: Acute pancreatitis (AP) is characterized by release of proteolytic enzymes from the pancreas and activation of the inflammatory cytokine cascade that mediates the systemic manisfestations of the disease. In fact, the peritoneal exudate that develops during AP attacks has been found to contain a number of biologically active components which may be harmful to the patient.
Aim: To investigate the effect of peritoneal lavage on the systemic inflammatory response in a rat model of severe AP.
Methods: AP was induced in male Wistar rats by intraductal 5% taurocholate injection. Peritoneal lavage was carried out by infusion of 200 ml of warm (37 °C) 1.5% glucose-based peritoneal dialysis fluid at a constant flow (50 ml/h). Animals were divided in 2 groups: Group I (n=16): Animals with AP treated by peritoneal lavage immediately after the induction of AP and Group II (n=16): Animals with AP not treated by peritoneal lavage. After 4 hours of AP induction serum levels of amylase, TNF-α, IL-6 and IL-10 were determined. Systemic lesions were analyzed by phosphorylation of liver mitochondria and pulmonary MPO determination.
Results: A significant decrease of TNF-α (7 ± 5 vs 32 ± 10 pg/ml) and IL-6 (141 ± 26 vs 258 ± 46 pg/ml) plasma levels was observed in animals submitted to peritoneal lavage (GI) when compared to animals that did not receive peritoneal lavage (GII) (p<0.05). Also, a significant increase of IL-10 (133 ± 44 vs 39 ± 8 pg/ml) plasma levels was observed in animals of GI when compared to GII (p<0.05). The group receiving peritoneal lavage had a significant reduction of liver mitochondria dysfunction: RCR (2.47 ± 0.08 vs 2.25 ± 0.06) and respiration state 4 (39.01 ± 2.29 vs 48.54 ± 3.28 nmol O2/mg prot/min) when compared to group not treated with peritoneal lavage (p<0.05). There were no significant differences on plasma amylase levels and pulmonary MPO between both groups.
Conclusion: These results indicate that peritoneal lavage attenuates the systemic inflammatory response by a reduction on plasma levels of TNF-α and IL-6, an increase of IL-10, and through a protective effect on uncoupling of mitochondrial oxidative phosphorylation in this model of experimental AP.