Chronic alcohol ingestion increases hepatic and pulmonary damage in experimental necrotizing pancreatitis

Background: In severe necrotizing pancreatitis (SNP) systemic complications as pancreat it is associated lung injury (PALI) are crucial for morbidity and mortality. In the presented study we evaluated the role of chronic alcohol ingestion on the development of PALI. Methods: Wistar rats were fed for 6 weeks with either alcohol or control diet. This was followed by induction of SNP by intraductal bile salt followed by intravenous caerulein infusion for 6 hours. Control animals received Ringer’s solution. Hepatic microcirculation was assessed after 6 hours. Analyses of tissue and serum samples were performed after 12 hours in additional animals of each group. Results: SNP-related pancreatic tissue damage was not affected by preceeding alcohol exposure. In contrast, SNP was associated with increased pulmonary MPO-levels in alcohol fed animals indicating an increased pulmonary inflammatory damage. Furthermore, alcohol pretreatment revealed increased hepatic microcirculatory disturbances with an impairment of microperfusion and increased sticking leukocytes to control animals with SNP. Serum IL-6 levels were increased after both, alcohol pretreatment and induction of SNP. Highest levels were observed in alcohol fed SNP animals. Portal venous IL-6 levels were higher compared to systemic venous levels. Conclusion: Chronic alcohol exposure increases pulmonary inflammatory damage in experimental SNP. This may be explained by alcohol-related liver damage with a consecutive hepatic IL-6 release and does not seem to reflect a local pancreatic phenomenon.