Literature DB >> 12890996

Nitric oxide regulates bacterial translocation in experimental acute edematous pancreatitis.

Mehmet Hakan Cevikel1, Hedef Ozgün, Sükrü Boylu, Ahmet Ender Demirkiran, Serhan Sakarya, Nil Culhaci.   

Abstract

BACKGROUND/AIMS: The role of nitric oxide (NO) in bacterial translocation (BT) associated with acute pancreatitis is controversial. We investigated the effects of the NO synthase substrate, L-arginine, and the NO synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on BT in caerulein-induced acute pancreatitis in rats.
METHODS: Acute pancreatitis was induced by subcutaneous injections of caerulein (12 microg/kg) at 6-hour intervals for 2 days. Subcutaneous injections of L-arginine (100 mg/kg) or L-NAME (10 mg/kg) were administeredonce daily for 2 days. At 48 h, pancreatic injury and BT to the mesenteric lymph nodes (MLN), liver, and peritoneum were assessed.
RESULTS: Compared with controls, rats that received caerulein injections alone had increased BT to the MLN and pancreatic inflammatory changes. L-Arginine significantly reduced the inflammation and BT caused by caerulein. L-NAME did not significantly alter pancreatic inflammation. Although caerulein + L-NAME-treated rats had increased BT to the peritoneum, MLN, and liver compared with controls, rates of BT did not significantly differ between caerulein alone- and caerulein + L-NAME-treated rats.
CONCLUSION: In acute edematous pancreatitis, BT is increased and is regulated by NO. NO substrates limit BT and pancreatic inflammation associated with acute pancreatitis, probably by their bactericidal actions and ability to improve pancreatic blood flow. Copyright 2003 S. Karger AG, Basel and IAP

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Year:  2003        PMID: 12890996     DOI: 10.1159/000071772

Source DB:  PubMed          Journal:  Pancreatology        ISSN: 1424-3903            Impact factor:   3.996


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