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1Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224; and 2Department of Chest Medicine, Faculty of Medicine, Ankara University, 06100 Ankara, Turkey
Submitted 12 February 2003 ; accepted in final form 15 May 2003
Patients with acute respiratory distress syndrome are at increased risk for
developing multiorgan system dysfunction. The goal of this study was to
establish an in vivo murine model to assess the differential effects of
ventilation-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 or
no intervention. Mean arterial pressure was continuously monitored during MV
and did not differ between groups. After 4 h, lung injury was assessed by
measurement of wet/dry lung weight, lung lavage protein concentration and cell
count, and histology. Concentration of IL-6, TNF-
, 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. Although 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 manifested lung injury and increased IL-6 and VEGFR2 in
lung, liver, and kidney, whereas 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 MV strategy has differential effects on
systemic inflammatory changes and thus may selectively predispose to systemic
organ dysfunction.
multiorgan system dysfunction; interleukin-6; tumor necrosis factor-; vascular endothelial growth factor; vascular endothelial growth factor receptor-2
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