Low tidal volume mechanical ventilation and oxidative stress in healthy mouse lungs

J Bras Pneumol. 2012 Jan-Feb;38(1):98-104. doi: 10.1590/s1806-37132012000100014.
[Article in English, Portuguese]

Abstract

Objective: Mechanical 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.

Methods: Twenty 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.

Results: In 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).

Conclusions: Our results show that short-term low V T MV can directly contribute to lung injury, generating oxidative stress and inflammation in healthy mouse lungs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / analysis
  • Inflammation / etiology
  • Inflammation / pathology*
  • Lipid Peroxidation / physiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Models, Animal
  • Oxidative Stress / physiology*
  • Random Allocation
  • Respiration, Artificial / adverse effects*
  • Respiration, Artificial / methods
  • Statistics, Nonparametric
  • Tidal Volume / physiology*
  • Tumor Necrosis Factor-alpha / physiology*
  • Ventilator-Induced Lung Injury / etiology*
  • Ventilator-Induced Lung Injury / metabolism
  • Ventilator-Induced Lung Injury / pathology

Substances

  • Biomarkers
  • Tumor Necrosis Factor-alpha