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Type: Artigo de periódico
Title: Pentoxifylline decreases tumor necrosis factor and interleukin-1 during high tidal volume
Author: Oliveira-Junior, I.S.
Pinheiro, B.V.
Silva, I.D.C.G.
Salomão, R.
Zollner, R.L.
Beppu, O.S.
Abstract: Tumor necrosis factor-alpha (TNF-alpha) is one of the most important proinflammatory cytokines which plays a central role in host defense and in the acute inflammatory response related to tissue injury. The major source of TNF-alpha are immune cells such as neutrophils and macrophages. We tested the hypothesis that pentoxifylline, a methylxanthine derivative, down-regulates proinflammatory cytokine expression during acute lung injury in rats. Male Wistar rats weighing 250 to 450 g were anesthetized ip with 50 mg/kg sodium thiopental and randomly divided into three groups: group 1 (N = 7): tidal volume (V T) = 7 ml/kg, respiratory rate (RR) = 50 breaths/min and normal saline infusion; group 2 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and normal saline infusion; group 3 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and pentoxifylline infusion. The animals were ventilated with an inspired oxygen fraction of 1.0, a positive end-expiratory pressure of 3 cmH2O, and normal saline or pentoxifylline injected into the left femoral vein. The mRNA of TNF-alpha rapidly increased in the lung tissue within 180 min of ventilation with a higher V T with normal saline infusion. The concentrations of inflammatory mediators were decreased in plasma and bronchoalveolar lavage (BAL) in the presence of higher V T with pentoxifylline infusion (TNF-alpha: plasma, 102.2 ± 90.9 and BAL, 118.2 ± 82.1; IL-1ß: plasma, 45.2 ± 42.7 and BAL, 50.2 ± 34.9, P < 0.05). We conclude that TNF-alpha produced by neutrophil influx may function as an alert signal in host defense to induce production of other inflammatory mediators.
Subject: Tumor necrosis factor-alpha
Acute lung injury
Editor: Associação Brasileira de Divulgação Científica
Citation: Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 36, n. 10, p. 1349-1357, 2003.
Rights: aberto
Identifier DOI: 10.1590/S0100-879X2003001000011
Date Issue: 1-Oct-2003
Appears in Collections:Unicamp - Artigos e Outros Documentos

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