[The pathogenesis of infection complicated by acute necrotizing pancreatitis: an experimental study]

To observe the injury of gut barrier function and intestinal bacterial translocation following acute necrotizing pancreatitis (ANP), and to investigate the pathogenesis of infection complicated by ANP.

Fifteen dogs were colonized with a strain of E. coli JM109 bearing ampicillin-resistant plasmid PUC18, then divided into two groups: control group (n = 7) and ANP group (n = 8). Acute necrotizing pancreatitis was induced by injection of sodium taurocholate and trypsin into the pancreatic duct.

In the ANP group, as compared with the control group, serum amylase level increased significantly, the lactulose/mannitol ratio was 2-12 times higher, blood and ileum diamine oxidase activity decreased significantly. E. coli population in intestinal mucosal flora increased, while bifidobacterium and lactobacillus reduced significantly. Bifidobacterium/E. coli ratio was reversed. Morphological study revealed areas of hemorrhage and necrosis in the pancreas and shedding of ileal villi. In the control group, blood cultures were negative, and no organism was found in organs except for mesenteric lymph nodes in two dogs. In the ANP group, blood and organ cultures were positive in all dogs and JM109 could be found uniformly too.

ANP impaired the gut barrier function, which led to bacterial translocation from the gut to the pancreas and other organs, serving as a primary source of infection secondary to ANP.