Hepatic contribution to circulating cytokine levels in severe acute pancreatitis in rats

The inflamed pancreas is one source of cytokine release during acute pancreatitis (AP). However, cytokines from other sites (e.g. liver or lung) may contribute to the multi-organ dysfunction syndrome that complicates severe AP. In this study, we determined the relative contributions of various possible sites during AP in rats. METHODS: 24 female rats were randomly allocated to 3 groups. A: control group (n=6); B: sham operation (intraductal saline infusion) (n=8); C: AP (intraductal infusion of 5% sodium-taurocholate) (n=10). Intraductal infusions were pressure ( < 20mmHg) and volume (0.5ml) controlled. Control animals were sacrificed at time zero. All other animals were sacrificed 2 hours after intraductal infusion. Blood samples were taken selectively from the iliac artery, the portal and hepatic vein. Cytokines were determined by rat specific ELISA. Endotoxin, since it is a potent stimulator of cytokine production, was assessed by a Limulus Amoebocyte Lysate assay. Histologic changes in the pancreas were scored in a blinded fashion (0 to 22, normal to most abnormal) by two investigators. Statistics: One way ANOVA or Mann-Whitney U-test. RESULTS: No cytokines were detectable in the control or sham group and no endotoxin was detectable in any serum sample. Histology confirmed hemorrhagic pancreatitis in group C (p < 0.001 vs group A or B). Cytokine values in pg/ml are mean ± SEM in group C: