Hyperoxia and Hypercapnic Acidosis Differentially Alter Nuclear Factor-κB Activation in Human Pulmonary Artery Endothelial Cells
Although ventilator-associated pulmonary injury, such as oxygen toxicity or barotrauma, has given rise to critical problems for mechanically ventilated patients with serious lung diseases, mechanical ventilation is an essential procedure to maintain appropriate tissue oxygenation, pH, and Pco2 in patients with respiratory distress (Dreyfuss and Saumon, 1998). In order to reduce the possibility of ventilator-associated pulmonary barotrauma, permissive hypercapnia has been applied as appropriate ventilatory support to acute respiratory distress syndrome (ARDS) (Feihl and Perret, 1994). In spite of the fact that there are some favorable prospective trials reporting that permissive hypercapnia improved mortality in patients with ARDS induced by heterogeneous background disorders (Hickling et al., 1994, Amato et al., 1998), efficacy and indication of this newly developed ventilator strategy are still controversial (Hudson, 1998). Permissive hypercapnia requires higher inspired oxygen concentration to maintain arterial oxygen tension than conventional mechanical ventilation mode and induces systemic hypercapnic acidosis for at least 48 hours (Carvahlo et al., 1997), thus arising the question whether hyperoxia and hypercapnic acidosis would exert a significant influence on sustained inflammation including ARDS.
KeywordsToxicity Glycerol Attenuation EDTA Glutathione
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