• Karla Maria Pereira Pires, Adriana Correa Melo, Manuella Lanzetti, Natália Vasconcelos Casquilho, Walter Araújo Zin, Luís Cristóvão Porto, and Samuel Santos Valença.
• Departamento de Histologia e Embriologia, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brasil.
• J Bras Pneumol. 2012 Jan 1; 38 (1): 98-104.

ObjectiveMechanical ventilation (MV) itself can directly contribute to lung injury. Therefore, the aim of the present study was to investigate early biomarkers concerning oxidant/antioxidant balance, oxidative stress, and inflammation caused by short-term MV in healthy mouse lungs.MethodsTwenty male C57BL/6 mice were randomly divided into two groups: MV, submitted to low tidal volume (V T, 6 mL/kg) MV for 30 min; and spontaneous respiration (SR), used as controls. Lung homogenate samples were tested regarding the activity of various antioxidant enzymes, lipid peroxidation, and TNF-α expression.ResultsIn comparison with the SR group, the MV group showed a significant decrease in the activity of superoxide dismutase (≈35%; p < 0.05), together with an increase in the activity of catalase (40%; p < 0.01), glutathione peroxidase (500%; p < 0.001), and myeloperoxidase (260%; p < 0.001), as well as a reduction in the glutathione/oxidized glutathione ratio (≈50%; p < 0.05) and an increase in TNF-α expression in the MV group. Oxidative damage, assessed by lipid peroxidation, was also greater in the MV group (45%; p < 0.05).ConclusionsOur results show that short-term low V T MV can directly contribute to lung injury, generating oxidative stress and inflammation in healthy mouse lungs.

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