Nitric oxide regulates bacterial translocation in experimental acute edematous pancreatitis

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 (12μg/kg) at 6-hour intervals for 2 days. Subcutaneous injections of L-arginine (100 mg/kg) orL-NAME (10 mg/kg) were administered once 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 sub-strates 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.