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Type: Artigo de periódico
Title: Role Of Substance P And Bradykinin In Acute Pancreatitis Induced By Secretory Phospholipase A2.
Author: Camargo, Enilton A
Ferreira, Tatiane
Ribela, Maria Teresa C P
de Nucci, Gilberto
Landucci, Elen C T
Antunes, Edson
Abstract: Secretory phospholipases A2 (sPLA2s) induce acute pancreatitis when injected into the common bile duct of rats. Substance P via neurokinin 1 (NK-1) receptors and bradykinin via B2 receptors are described to play important roles in the pathophysiology of acute pancreatitis. This study was undertaken to evaluate the role of substance P and bradykinin in the sPLA2-induced pancreatitis. Rats were submitted to the common bile duct injection of sPLA2 obtained from Naja mocambique mocambique venom at 300 microg/kg. At 4 hours thereafter, measurement of pancreatic plasma extravasation, pancreatic and lung myeloperoxidase (MPO), serum amylase, and serum tumor necrosis factor alpha levels were evaluated. Injection of sPLA2 significantly increased all parameters evaluated. Pretreatment with either the NK-1 receptor antagonist SR140333 or the B2 receptor antagonist icatibant largely reduced the increased pancreatic plasma extravasation and circulating levels of tumor necrosis factor alpha. Both treatments partly reduced the MPO levels in the pancreas, whereas in the lungs, icatibant was more efficient to reduce the increased MPO levels. In addition, icatibant largely reduced the serum levels of amylase, whereas SR140333 had no significant effect. We concluded that NK-1 and B2 receptors can regulate important steps in the local and remote inflammation during acute pancreatitis induced by sPLA2.
Subject: Acute Disease
Bradykinin B2 Receptor Antagonists
Disease Models, Animal
Neurokinin-1 Receptor Antagonists
Phospholipases A2, Secretory
Rats, Wistar
Receptor, Bradykinin B2
Receptors, Neurokinin-1
Substance P
Tumor Necrosis Factor-alpha
Citation: Pancreas. v. 37, n. 1, p. 50-5, 2008-Jul.
Rights: fechado
Identifier DOI: 10.1097/MPA.0b013e3185d9b9b
Date Issue: 2008
Appears in Collections:Unicamp - Artigos e Outros Documentos

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