Objective: To evaluate the effect of enteral nutrition (EN) in attenuating bacterial and/or endotoxin translocation, maintaining immune responsiveness, and improving outcome in early acute pancreatitis (AP) in Wistar male rats.
Design: Acute pancreatitis was induced in rats receiving total parenteral nutrition (TPN) (AP/TPN group) (n=34) and EN (AP/EN group) (n=35) by pressure injection of 1% deoxycholate into the biliopancreatic duct (0.6 mg/kg of body weight). Rats in the sham/TPN and sham/EN groups (n=10 each) underwent laparotomy without induction of AP. Catheters for TPN and EN were placed into the external jugular vein and jejunum, respectively. Rats were infused with Ringer lactate solution for 48 hours followed by TPN in the AP/TPN and sham/TPN groups, and EN in the AP/EN and sham/EN groups until day 7. The fluid volume and energy (calories) intake were similar in all groups.
Setting: Medical school research laboratory.
Main outcome measures: Survival, blood endotoxin level, villus height, 5-bromo-2'-deoxyuridine (BrdU) uptake in the jejunum and ileum, bacterial culture of mesenteric lymph nodes, and CD4/CD8 ratio of T cells in mesenteric lymph nodes, spleen, and peripheral blood.
Results: There was no difference in survival and pancreatic healing between the AP/TPN and AP/EN groups. Colony-forming units of the mesenteric lymph nodes and the endotoxin level were significantly lower in the AP/EN group than in the AP/TPN group (P<.05). Villus height and BrdU intake was significantly higher in the AP/EN group than in the AP/TPN group (P<.05). The CD4/CD8 ratio of T cells in spleen and peripheral blood was higher in the AP/EN group than in the AP/TPN group (P<.05), whereas there was no difference in mesenteric lymph nodes.
Conclusions: Jejunal administration of EN is well tolerated in early AP, maintains immune responsiveness and gut integrity, and reduces bacterial and/or endotoxin translocation. However, compared with TPN, EN does not improve outcome. These results suggest that factors other than bacterial and/or endotoxin translocation may be responsible for mortality in this rat model of early AP. However, additional studies of both early bacterial and/or endotoxin translocation and late assessment of outcome are indicated.