Introduction Large-tidal volume (V T ) 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 V T and hyperoxia are unclear. We hypothesized that the addition of hyperoxia to large-V T ventilation would increase neutrophil infiltration by upregulation of the cytokine macrophage inflammatory protein-2 (MIP-2) and would increase apoptosis via the mitogen-activated protein kinase pathways.

In patients with symptomatic malignant pleural effusion, measurement of the elastance of the pleural space is a simple and effective method for the diagnosis of trapped lung and prediction of the outcome of chemical pleurodesis with bleomycin.

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