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Copyright ©ERS Journals Ltd 2005
VEGF levels in the alveolar compartment do not distinguish between ARDS and hydrostatic pulmonary oedema
1 Division of Allergy, Pulmonary and Critical Care Medicine, Dept of Medicine, Vanderbilt University School of Medicine, Nashville, TN, 2 Division of Pulmonary and Critical Care Medicine, Weill Medical College of Cornell University, New York, NY, 3 Cardiovascular Research Institute, 4 Dept of Medicine and Anesthesia, University of California, San Francisco, CA, USA
CORRESPONDENCE: L. B. Ware, T1218 MCN, 1161 21st Avenue South, Vanderbilt University School of Medicine, Nashville, TN 37232-2650, USA. Fax: 1 6153437448. E-mail: lorraine.ware@vanderbilt.edu
Keywords: Acute pulmonary oedema, acute respiratory distress syndrome
Received: September 12, 2004
Accepted February 25, 2005
Although overexpression of vascular endothelial growth factor (VEGF) 165 in the lung causes pulmonary oedema, its role in human acute lung injury (ALI) is unclear. VEGF levels are reported to be lower in bronchoalveolar lavage from ALI patients compared with normals, but these studies did not include a comparably ill control group with noninflammatory pulmonary oedema.
The current authors hypothesised that VEGF levels in pulmonary oedema fluid would be lower in ALI patients compared with control patients with severe hydrostatic pulmonary oedema. VEGF was measured in pulmonary oedema fluid and plasma from 56 patients with ALI and 46 controls with severe hydrostatic pulmonary oedema.
Pulmonary oedema fluid levels of VEGF did not differ between patients with hydrostatic oedema (median 799 pg·mL–1, interquartile range (IQR) 226–2,281) and ALI (median 507, IQR 0.8–1,031). Plasma levels were also the same (median 20.5 pg·mL–1, IQR 0–152 versus 4.8, IQR 0–99.8). There was no association between plasma or oedema fluid VEGF levels and outcomes including mortality.
Vascular endothelial growth factor levels in pulmonary oedema fluid were depressed both in acute lung injury and hydrostatic pulmonary oedema. The decrease in air space concentrations of vascular endothelial growth factor in acute lung injury may not be a function of the degree of lung injury, but rather may result from alveolar flooding.
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