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BACKGROUND: Though inhaled nitric oxide (iNO) improved oxygenation but had no effect on mortality in randomized clinical trial for acute respiratory distress syndrome (ARDS), its efficacy in modulation of inflammation and antioxidant capability in airway and alveolar epithelial cells in mature lungs remains to be verified. As iNO is usually used in hyperoxic condition, it may alter surfactant lipid de novo synthesis in inflammatory lung. Despite the fact that NO may potentiate damage to surfactant proteins and inhibit surfactant phospholipid synthesis, iNO is still considered an alternative and encouraging therapy in intractable respiratory failure to obviate more invasive and expensive strategies. OBJECTIVE: To investigate whether hyperoxia and/or inhaled nitric oxide (iNO) may affect de novo synthesis of phosphatidylcholine (PC) in mature lungs with inflammatory injury. METHODS: Healthy adult S-D rats were first assigned into a normal control group (C) or a group with lipopolysaccharides (2 mg/kg iv)
BACKGROUND: Though inhaled nitric oxide (iNO) improved oxygenation but had no effect on mortality in randomized clinical trial for acute respiratory distress syndrome (ARDS), its efficacy in modulation of inflammation and antioxidant capability in airway and alveolar epithelial cells in mature lungs remains to be verified. As iNO is usually used in hyperoxic condition, it may alter surfactant lipid de novo synthesis in inflammatory lung. Despite the fact that NO may potentiate damage to surfactant proteins and inhibitory phospholipid synthesis, iNO is still considered an alternative and encouraged therapy OBJECTIVE: To investigate whether hyperoxia and / or inhaled nitric oxide (iNO) may affect de novo synthesis of phosphatidylcholine (PC) in mature lungs with inflammatory injury. METHODS: Healthy adult SD rats were first assigned into a normal control group (C) or a group with lipopolysacchar ides (2 mg / kg iv)