Background: Reduced bioactive vascular endothelial growth factor (VEGF) has been demonstrated in
several inflammatory lung conditions including the acute respiratory distress syndrome (ARDS). sVEGFR-1,
a soluble form of VEGF-1 receptor, is a potent natural inhibitor of VEGF. We hypothesised that sVEGFR-1
plays an important role in the regulation of the bioactivity of VEGF within the lung in patients with ARDS.
Methods: Forty one patients with ARDS, 12 at risk of developing ARDS, and 16 normal controls were
studied. Bioactive VEGF, total VEGF, and sVEGFR-1 were measured by ELISA in plasma and
bronchoalveolar lavage (BAL) fluid. Reverse transcriptase polymerase chain reaction for sVEGFR-1 was
performed on BAL cells.
Results: sVEGFR-1 was detectable in the BAL fluid of 48% (20/41) of patients with early ARDS (1.4–
54.8 ng/ml epithelial lining fluid (ELF)) compared with 8% (1/12) at risk patients (p = 0.017) and none of
the normal controls (p = 0.002). By day 4 sVEGFR-1 was detectable in only 2/18 ARDS patients
(p = 0.008). Patients with detectable sVEGFR-1 had lower ELF median (IQR) levels of bioactive VEGF than
those without detectable sVEGFR-1 (1415.2 (474.9–3192) pg/ml v 4761 (1349–7596.6) pg/ml, median
difference 3346 pg/ml (95% CI 305.1 to 14711.9), p = 0.016), but there was no difference in total VEGF
levels. BAL cells expressed mRNA for sVEGFR-1 and produced sVEGFR-1 protein which increased
following incubation with tumour necrosis factor a.
Conclusion: This study shows for the first time the presence of sVEGFR-1 in the BAL fluid of patients with
ARDS. This may explain the presence of reduced bioactive VEGF in patients early in the course of ARDS
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