Hyperoxic acute lung injury and ventilator-induced/associated lung injury: new insights into intracellular signaling pathways.
In patients with acute respiratory distress syndrome (ARDS), supportive therapy with mechanical ventilation and oxygen is often life saving. Further acute lung injury however, is an unfortunate consequence of oxygen therapy as well as mechanical injury secondary to ventilator induced/associated lung injury (VI/ALI). In this issue of Critical Care, Li et al. expand on the intra-cellular signaling pathways regulating interactions between injury cascades resulting from hyperoxia and high tidal volume ventilation. The findings, suggest that interference or cooperation of different signals may have critical consequences as evidenced by indices of increased lung inflammation, microvascular permeability, and lung epithelial apoptotic cell death.
Dos Santos
Claudia C
CC
Saint Michael's Hospital, Department of Critical Care Medicine 30, Bond Street 4-008, Toronto, ON M5G 1W8, Canada. dossantosc@smh.toronto.on.ca
D016207:Cytokines / Q000096:biosynthesis; D006801:Humans; D018496:Hyperoxia / Q000209:etiology / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism*; D008171:Lung Diseases / Q000209:etiology* / Q000378:metabolism*; D020556:Neutrophil Infiltration; D009687:Nuclear Proteins / Q000378:metabolism*; D012121:Respiration, Artificial / Q000009:adverse effects*; D012128:Respiratory Distress Syndrome / Q000150:complications / Q000628:therapy*; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D016207:Cytokines; D007378:Interleukins; D009687:Nuclear Proteins; D014409:Tumor Necrosis Factor-alpha