• Xiang-qing Xiong, Wan-tie Wang, Liang-rong Wang, Li-da Jin, and Li-na Lin.
• Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical College, Wenzhou, Zhejiang, China.
• Int. Immunopharmacol. 2012 Jul 1;13(3):280-3.

BackgroundMechanical ventilation may paradoxically cause lung injury. Protective mechanical ventilation strategy utilizing low tidal volume and high frequency has been shown to attenuate inflammation and reduce mortality in non-diabetic patients. The purpose of this present study was to observe the effects of diabetes on inflammation and lung injury in mice with protective ventilation strategy.MethodsForty mice were included in our study. The mice in Group Dia-MV and Con-MV were subjected to 4 hour-ventilation. And the mice in Group Dia-SB and Con-SB were exposed to room air breathing spontaneously for 4h. Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10), superoxide dismutase (SOD) and malondialdehyde (MDA) levels in serum were detected and the expression of inflammatory cytokine mRNA was also determined in lung tissue. Lung damage was assessed using a modified lung injury score.ResultsThe serum levels of TNF-α, IL-6, and IL-10 in Group Dia-MV were significantly higher than those in Group Dia-SB or Group Con-MV or Group Con-SB (P<0.05). Quantitative RT-PCR analysis of pro-inflammatory cytokines in lung homogenates presented similar results. The mice in Group Dia-MV suffered obvious lung histological changes, whose lung injury scores were significantly higher in Group Dia-SB as compared to Group Con-SB , Group Con-MV or Group Dia-SB (P<0.05).ConclusionsDiabetes increased the inflammation reaction and associated lung injury in mice in spite of the protective mechanical ventilation strategy based on low tidal volumes and high frequency.Copyright © 2012 Elsevier B.V. All rights reserved.

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