Nitric oxide regulates bacterial translocation in experimental acute edematous pancreatitis
Autor: | Hedef Özgün, Nil Culhaci, Ahmet Ender Demirkiran, Mehmet Hakan Çevikel, Serhan Sakarya, Şükrü Boylu |
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Rok vydání: | 2003 |
Předmět: |
Male
medicine.medical_specialty Injections Subcutaneous Endocrinology Diabetes and Metabolism Bacterial translocation Pharmacology Arginine Nitric Oxide Nitric oxide chemistry.chemical_compound Internal medicine No synthase Animals Edema Medicine Rats Wistar Pancreas Ceruletide Hepatology business.industry Gastroenterology medicine.disease Rats NG-Nitroarginine Methyl Ester Endocrinology Liver Pancreatitis chemistry Bacterial Translocation Acute Disease Acute pancreatitis Lymph Nodes Nitric Oxide Synthase Peritoneum business |
Zdroj: | Pancreatology. 3:329-335 |
ISSN: | 1424-3903 |
Popis: | 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.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.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.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. |
Databáze: | OpenAIRE |
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