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1 Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Chest Medicine, Ankara University Faculty of Medicine, Ankara, Turkey
2 Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: pbecker1{at}jhmi.edu.
Patients with ARDS are at increased risk for the development of multi-organ system dysfunction. The goal of this study was to establish an in vivo murine model to assess the differential effects of ventilator-protective strategies on the development of acute lung injury and systemic organ inflammation. C57B/6 mice were randomized to mechanical ventilation (MV) with conventional, high (17 ml/kg) or protective, low (6 ml/kg) tidal volume (VT), after intratracheal hydrochloric acid (HCl) or no intervention. Mean arterial pressure was continuously monitored during MV, and did not differ between groups. After 4 hours, lung injury was assessed by measurement of wet/dry lung weight, lung lavage protein concentration and cell count, and histology. Concentration of interleukin-6 (IL-6), tumor necrosis factor-
(TNF-), vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR2) was measured in lung, liver, kidney and heart. Results were compared with control, spontaneously breathing mice. Lung injury and altered pulmonary cytokine expression were not detected after MV of healthy mice with low or high VT. While MV did not significantly alter IL-6 or TNF- in systemic organs, VEGF concentration significantly increased in liver and kidney. After acid aspiration, mice ventilated with high VT manifest lung injury and increased IL-6 and VEGFR2 in lung, liver and kidney, while VEGF increased only in liver and kidney. MV with low VT after acid aspiration attenuated lung injury, both IL-6 and VEGFR2 expression in lung and systemic organs, and hepatic, but not renal, increased VEGF. Our data suggest that mechanical ventilatory strategy has differential effects on systemic inflammatory changes, thus may selectively predispose to systemic organ dysfunction.
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