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Background: Ventilator-induced lung injury (VILI) sustained during mechanical ventilator support is still a cause of ahigh rate of morbidity and mortality in intensive care units and in operating rooms. VILI is characterized by pulmonaryinflammation that appears to be mediated by proinflammatory cytokines. This study investigates whether the volatile anestheticsevoflurane has an anti-inflammatory effect that attenuates VILI. Methods: Twenty one male rabbits were anesthetized and were mechanically ventilated with 50% oxygen at a peak inspiratorypressure (PIP) of 10 cmH2O, I : E ratio of 1 : 4, and positive end expiratory pressure of 5 cmH2O. All animalswere randomly assigned to one of three groups that were ventilated for 5 h with 10 cmH2O of PIP (Sham group, n = 7);30 cmH2O of PIP (Control group, n = 7); or 30 cmH2O of PIP and 0.8 vol% sevoflurane (Sevoflurane group, n = 7). Thewet/dry weight (W/D) ratio and histopathology of the lung; concentration of interleukin-8 (IL-8) in the bronchoalveolarlavage fluid; and activation of extracellular signal-regulated kinases (ERK) 1/2, p38 mitogen-activated protein kinase, andAkt were measured in the lung tissue after completing the protocol. Results: Histopathology indicated that the sevoflurane group showed fewer inflammatory cells and architectural changesthan the control group did. The W/D ratio [(5.36 ± 0.13) versus (6.61 ± 0.20)], expression of IL-8 [(144.08 ± 14.61) versus(228.56 ± 15.13) pg/ml] and phosphorylation of ERK1/2 and Akt decreased significantly in the sevoflurane group relativeto the control group. Conclusions: Sevoflurane attenuates VILI in rabbits mainly by inhibiting expression of IL-8, and Sevoflurane-inducedinhibition of phosphorylated ERK1/2 and Akt might be a possible pathway for protection.

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