Infections from enteric bacteria are a major cause of morbidity and mo
rtality during acute pancreatitis (AP), but the pathways by which thes
e organisms reach distant organs remains speculative. Experiments were
conducted to determine if bacterial translocation could be a mechanis
m for infection during this disease. AP was induced in Lewis rats by i
.v. infusion of caerulein (experiment I) or ligation of the head of th
e pancreas (experiment II). In a third experiment, rats were gavaged w
ith 1 x 10(8) C-14-radiolabeled Escherichia coli and pancreatitis was
induced with caerulein. Results in all three experiments showed that A
P increased the number of viable bacteria recovered in peritoneal flui
d, mesenteric lymph nodes (MLN), liver, lungs, and pancreas. Radionucl
ide counting indicated that AP enhanced the gut permeability to C-14 E
. coli. To estimate the impact of AP on the magnitude of translocation
and on the ability of the host to clear bacteria, the nuclide and col
ony-forming units (CFU) ratios were calculated between animals with an
d without AP. Blood, peritoneal fluid, and MLN had the highest nuclide
ratio. During AP, these tissues may be the principal routes for bacte
rial spreading from the gut lumen. Peritoneal fluid, pancreas, and lun
g were the tissues with the highest CFU ratio. Bacterial killing abili
ty of these tissues is likely impaired during AP.