• Guizhi Du, Shurong Wang, Zhuo Li, and Jin Liu.
• From the *Laboratory of Anesthesia and Critical Care Medicine, Department of Anesthesiology, West China Hospital of Sichuan University, Chengdu, Sichuan, China; †Department of Neurology, The Second People's Hospital of Chengdu, Chengdu, Sichuan, China; and ‡Department of Pharmacy, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.
• Anesth. Analg. 2017 May 1; 124 (5): 1555-1563.

BackgroundIn animal models, both sevoflurane and propofol protect against acute lung injury (ALI), especially when administered prior to ALI onset. We hypothesized that when compared to propofol, sevoflurane administration after the onset of acute respiratory distress syndrome would mitigate oleic acid (OA)-induced ALI in dogs.MethodsDogs were randomly assigned to receive intravenous OA to induce ALI (n = 7 for each OA group) or saline as an OA control (n = 6 for each control). Dogs were then mechanically ventilated for 6 hours during which propofol (5 mg/kg/h) or sevoflurane (1.0 minimum alveolar concentration) was administered for sedation. Study end points included PO2/FIO2 ratio, pulmonary arterial pressure, pulmonary edema, histology, and tumor nuclear factor-α.ResultsIn OA-injured animals, oxygenation was worse at 1, 2, 3, and 4 hours after 6-hour mechanical ventilation in sevoflurane-sedated animals compared with propofol-sedated animals, with mean difference (95% confidence interval; propofol minus sevoflurane) of 75 (39-111), 87 (55-119), 66 (44-87), and 67 (27-107) mm Hg for the respective time points. However, sevoflurane reduced the elevated pulmonary arterial pressure and vascular resistance, attenuated pulmonary edema as evidenced by reduced extravascular lung water index, and decreased tumor nuclear factor-α and diffuse alveolar damage score compared with propofol in the OA-injured lungs.ConclusionsWhen compared with propofol, sevoflurane attenuates OA-induced lung damage. However, despite this effect on lung histology and inflammation, sevoflurane worsened oxygenation in OA-induced ALI, possibly via inhibition of hypoxic pulmonary vasoconstriction.

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