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1 Department of Anaesthetics and Intensive Care, Imperial College London, Chelsea and Westminster Hospital, London, United Kingdom
2 Department of Histopathology, Royal Brompton Hospital, London, United Kingdom
* To whom correspondence should be addressed. E-mail: m.takata{at}imperial.ac.uk.
Mechanical ventilation has been demonstrated to exacerbate lung injury, and a sufficiently high tidal volume can induce injury in otherwise healthy lungs. However it remains controversial whether injurious ventilation per se, without preceding lung injury, can initiate cytokine-mediated pulmonary inflammation. To address this, we developed an in vivo mouse model of acute lung injury produced by high tidal volume (VT) ventilation. Anesthetised C57BL6 mice were ventilated at high VT (34.5±2.9ml/kg, mean±SD) for a duration of 156±17 minutes until mean blood pressure fell below 45mmHg (Series 1); high VT for 120 minutes (Series 2); or low VT (8.8±0.5ml/kg) for 120 or 180 minutes (Series 3). High VT produced progressive lung injury with a decrease in respiratory system compliance, increase in protein concentration in lung lavage fluid, and lung pathology showing hyaline membrane formation. High VT ventilation was associated with increased tumor necrosis factor-
(TNF-) in lung lavage fluid at the early stage of injury (Series 2) but not the later stage (Series 1). In contrast lavage fluid macrophage inflammatory protein-2 (MIP-2) was increased in all high VT animals. Lavage fluid from high VT animals contained bioactive TNF- by WEHI bioassay. Low VT ventilation induced minimal changes in physiology and pathology with negligible TNF- and MIP-2 proteins and TNF- bioactivity. These results demonstrate that high VT ventilation in the absence of underlying injury induces intrapulmonary TNF- and MIP-2 expression in mice. The apparently transient nature of TNF- upregulation may help explain previous controversy regarding the involvement of cytokines in ventilator-induced lung injury.
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