Abstract
Methods: Twenty-fourSwiss male mice were randomly divided into four groups: glutamine group (GLN), glutamine + L-NAME group (LN), sham group and intestinal obstruction group (IO). The glutamine animals received glutamine solution (500mg×kg 1×d 1) by gavage for 7 days before surgery, while L-NAME animals received glutamine plus L-NAME (nitric oxide synthase inhibitor) 10mg/kg. The diet was isocaloric and isoproteic. On the 8th day, the animals were gavaged with a suspension containing 108 UFC/mL of E. coli labeled with 99mTc. Ninety minutes later, the animals were anesthetized and terminal ileum was isolated and ligated. The sham group underwent laparotomy only. The animals were anesthetized 18 h after surgery for blood collection and were then euthanized. Blood, mesenteric lymph nodes (MLN), liver, spleen and lungs were removed for radioactivity determination. The small intestine was removed, suspended in saline buffer and centrifuged. The supernatant fluid was collected for IgA determination by ELISA. Statistical analyses were performed using KruscalWallis and ANOVA. Significance was considered when p 0.05. Results: BT was significantly higher in LN and IO groups, while animals that received only glutamine showed significantly reduced levels of BT in all investigated organs when compared with IO and LN groups (p < 0.05). SIgA levels were similar for GLN and LN groups (1185.5±108; 1346±155.1 respectively) and higher (p < 0.05) than IO group (622±75.5). Conclusion: L-NAME increased BT, suggesting that NO is an important substrate derived from glutamine which prevents BT.
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