Abstract

Cree et al. have detected intrapulmonary vascular endothelial growth factor (VEGF) levels far higher than in the plasma and speculate that these observations (along with the IL-8 findings) indicate subclinical lung injury following oesophageal surgery. However, although some studies have shown only modest BAL VEGF levels (240 pg.ml−1[1]), others have demonstrated significant levels of VEGF of more than 5.5 ng.ml−1in the epithelial lining fluid [2, 3], even though urea dilution methods were used to correct for BAL dilution. Indeed, in one of these studies [2], intrapulmonary levels of VEGF were found to be 500 times that of plasma. The reason for such high levels in normal subjects remains to be clarified. Observational human studies have highlighted a signficant intrapulmonary fall in VEGF levels in ARDS and a rise in plasma VEGF levels [3, 4]. It is possible that the loss of intrapulmonary VEGF is of greater biological significance in ARDS than its abundance in the normal state but further studies will ascertain this. The situation is still further complicated with VEGF in that the ELISA only detects two of the soluble VEGF isoforms, taking no account of the cell-associated physiologically active isoforms. In addition, smoking and increasing age are associated with reduced BAL VEGF levels [5] and comorbidity with, for example, cancer may profoundly alter VEGF levels, given the strong link between VEGF and angiogenesis. In conclusion, high BAL VEGF levels (unlike IL-8) may not necessarily indicate subclinical lung injury and the understanding of intraplumonary VEGF with respect to lung injury is still in its infancy.

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