One-lung overventilation does not induce inflammation in the normally ventilated contralateral lung

Respir Physiol Neurobiol. 2008 Jun 30;162(1):100-2. doi: 10.1016/j.resp.2008.04.009. Epub 2008 Apr 22.

Abstract

The aim was to assess whether induction of ventilator-induced lung injury (VILI) in one lung triggers a concomitant inflammatory response in the normally ventilated contralateral lung. To this end, a differential ventilator was used in 6 rats. One lung was normally ventilated (3.5 ml/kg b.w.) and the contralateral lung was overstretched (15 ml/kg b.w.). Six control rats were normally ventilated (3.5 ml/kg b.w. each lung). After 3h, edema and gene expression of MIP-2 in the lung, and plasma and liver TNF-alpha were assessed. Overexpression of MIP-2 and edema were found in the overventilated lung but not in the normally ventilated contralateral lung. No detectable levels of circulating and liver TNF-alpha were detected. These data do not support the hypothesis of an early positive feedback in the lung inflammation during the mechanical ventilation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chemokine CXCL2 / genetics
  • Chemokine CXCL2 / metabolism
  • Functional Laterality / physiology*
  • Gene Expression Regulation / physiology
  • Inflammation / etiology*
  • Inflammation / metabolism
  • Liver / metabolism
  • Lung / physiopathology*
  • Male
  • Rats
  • Rats, Wistar
  • Respiration*
  • Respiration, Artificial / adverse effects*
  • Statistics, Nonparametric
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Chemokine CXCL2
  • Tumor Necrosis Factor-alpha