Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury
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چکیده
منابع مشابه
Mitogen-Activated Protein Kinases Regulate Susceptibility to Ventilator-Induced Lung Injury
BACKGROUND Mechanical ventilation causes ventilator-induced lung injury in animals and humans. Mitogen-activated protein kinases have been implicated in ventilator-induced lung injury though their functional significance remains incomplete. We characterize the role of p38 mitogen-activated protein kinase/mitogen activated protein kinase kinase-3 and c-Jun-NH(2)-terminal kinase-1 in ventilator-i...
متن کاملHyperoxia increases ventilator-induced lung injury via mitogen-activated protein kinases: a prospective, controlled animal experiment
INTRODUCTION Large-tidal volume (VT) mechanical ventilation and hyperoxia used in patients with acute respiratory distress syndrome can damage pulmonary epithelial cells through lung inflammation and apoptotic cell death. Hyperoxia has been shown to increase ventilator-induced lung injury, but the mechanisms regulating interaction between large VT and hyperoxia are unclear. We hypothesized that...
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Lung ischemia-reperfusion (I-R) is an important model of oxidant-mediated acute lung and vascular injury. Heme oxygenase-1 (HO-1) is a cytoprotective gene that is markedly induced by lung I-R injury. HO-1 mRNA is increased in mouse lung after 30 min of lung hilar clamping (ischemia) followed by 2-6 h of unclamping (reperfusion) compared with control mice. In a variety of vascular cell types, HO...
متن کاملLung development and susceptibility to ventilator-induced lung injury.
RATIONALE Ventilator-induced lung injury has been predominantly studied in adults. OBJECTIVES To explore the effects of age and lung development on susceptibility to such injury. METHODS Ex vivo isolated nonperfused rat lungs (infant, juvenile, and adult) were mechanically ventilated where VT was based on milliliters per kilogram of body weight or as a percentage of the measured total lung ...
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ژورنال
عنوان ژورنال: PLoS ONE
سال: 2008
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0001601