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Type: Artigo de periódico
Title: Role Of Nitric Oxide On The Increased Vascular Permeability And Neutrophil Accumulation Induced By Staphylococcal Enterotoxin B Into The Mouse Paw.
Author: Franco-Penteado, C F
Desouza, I
Teixeira, S A
Ribeiro-DaSilva, G
De Nucci, G
Antunes, E
Abstract: The role of nitric oxide (NO) on the increase in vascular permeability and neutrophil migration induced by staphylococcal enterotoxin B (SEB; 25 microgram/paw) in the mouse was investigated in this study. The NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) [but not its inactive enantiomer N(omega)-nitro-D-arginine methyl ester (D-NAME)], given intravenously (25-100 micromol/kg) or subplantarly (0.25-1.0 micromol/paw), reduced SEB-induced paw oedema significantly. A similar response was observed with aminoguanidine, given either intravenously (200-600 micromol/kg) or subplantarly (2 micromol/paw). In contrast to paw oedema, the plasma exudation in response to SEB was not affected by the subplantar injection of L-NAME or aminoguanidine. The inhibition of oedema and plasma exudation by systemic treatment with L-NAME or aminoguanidine was reversed by co-injection of the vasodilator iloprost (0.3 nmol/paw). Subplantar injection of SEB (25 microgram/paw) increased by 69% the myeloperoxidase (MPO) activity of SEB-treated paws, indicating the presence of neutrophils. Intravenous (12.5-50 micromol/kg) or subplantar (0.125-0.5 micromol/paw) administration of L-NAME (but not of its inactive enantiomer, D-NAME) largely reduced the MPO activity in SEB-treated paws. Similarly, intravenous (200-600 micromol/kg) or subplantar (2 micromol/paw) administration of aminoguanidine significantly reduced the MPO values of the SEB-injected paws. The vasodilator iloprost (0.3 nmol/paw) completely reversed the inhibition by L-NAME or aminoguanidine of the MPO activity in SEB-injected paws. Our results show that the increased vascular permeability and neutrophil accumulation in response to subplantar injection of SEB in the mouse are inhibited by L-NAME and aminoguanidine by mechanisms probably involving reduction of local microvascular blood flow.
Subject: Animals
Capillary Permeability
Disease Models, Animal
Foot Diseases
Nitric Oxide
Nitric Oxide Synthase
Citation: Biochemical Pharmacology. v. 61, n. 10, p. 1305-11, 2001-May.
Rights: fechado
Date Issue: 2001
Appears in Collections:Unicamp - Artigos e Outros Documentos

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