Abstract
Background: Acid aspiration induces lung injury by causing an intense inflammatory reaction. Neutrophils are attracted by various cytokines, such as TNF beta, and release reactive oxygen species, which then cause acute lung injury. Endothelin antagonists, such as bosentan, have been found to possess anti-inflammatory properties. Materials and methods: We performed a prospective, randomised, ...
Abstract
Background: Acid aspiration induces lung injury by causing an intense inflammatory reaction. Neutrophils are attracted by various cytokines, such as TNF beta, and release reactive oxygen species, which then cause acute lung injury. Endothelin antagonists, such as bosentan, have been found to possess anti-inflammatory properties. Materials and methods: We performed a prospective, randomised, controlled study to evaluate the effects of bosentan in a rat model of acid-induced lung injury. Sprague-Dawley rats underwent sevoflurane anaesthesia; lung injury was then induced by instillation of 1.2 mL/kg, 0.1 M hydrochloric acid. The lungs were ventilated for 6 h and then randomised into three groups: bosentan 30 mg/kg body weight, 90 mg/kg body weight or sodium chloride, each applied immediately after acid aspiration via a gastric tube. Results: After induction of acute lung inflammation, the production of reactive oxyger, species by PMN following stimulation with FMLP increased significantly. Comparison of pre-treatment and post-treatment in the 90 mg/kg bosentan treatment group did not show a significant increase of reactive oxygen species following stimulation with FMLP. A comparison of the absolute difference of the MESF demonstrated a significant difference between the control group and the group treated with 90 mg/kg bosentan. Conclusions: Bosentan administration at 90 mg/kg body weight reduced the release of reactive oxygen species after 360 min in acid aspiration-induced lung injury in rats. (C) 2008 Elsevier Ltd. All rights reserved.
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