In:
Anesthesia & Analgesia, Ovid Technologies (Wolters Kluwer Health), Vol. 124, No. 5 ( 2017-05), p. 1555-1563
Abstract:
In 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. METHODS: Dogs 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 P o 2 /F io 2 ratio, pulmonary arterial pressure, pulmonary edema, histology, and tumor nuclear factor-α. RESULTS: In 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. CONCLUSIONS: When 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.
Type of Medium:
Online Resource
ISSN:
0003-2999
DOI:
10.1213/ANE.0000000000002034
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2017
detail.hit.zdb_id:
2018275-2
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