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Eur Respir J 2001; 18:100-106
Copyright ©ERS Journals Ltd 2001


Vascular endothelial growth factor synthesis in the acute phase of experimental and clinical lung injury

B. Maitre, S. Boussat, D. Jean, M. Gouge, L. Brochard, B. Housset, S. Adnot and C. Delclaux

INSERM Unité 492, Dépt de Physiologie and Services de Réanimation Médicale et Pneumologie, Hôpital Henri-Mondor, Créteil, France

CORRESPONDENCE: C. Delclaux, INSERM U492, Faculté de Médecine, 8, rue du Général Sarrail, 94010, Créteil, France. Fax: 33 148981777

Keywords: acute respiratory distress syndrome, animal study, bronchoalveolar lavage, human study, Pseudomonas aeruginosa pneumonia

Received: August 29, 2000
Accepted January 31, 2001

Vascular endothelial growth factor (VEGF) is a potent angiogenic and endothelial survival factor, which is abundantly expressed in the normal lung. Conceivably, VEGF may be released by numerous cell types found around the airspaces, including alveolar type 2 cells, alveolar macrophages, and polymorphonuclear neutrophils.

Using a bacteria-induced lung injury model in rats, VEGF expression in lung was investigated. Both VEGF protein and VEGF messenger ribonucleic acid (mRNA), 4 and 24 h after bacterial challenge (Pseudomonas aeruginosa), were decreased compared with sham rats.

VEGF protein was also investigated in bronchoalveolar lavage (BAL) from patients studied within 7 days of acute respiratory distress syndrome (ARDS) onset and in patients without ARDS. VEGF protein levels in BAL were decreased in patients with ARDS versus those without (14.3±11.1 pg·mL–1 versus 76.8±51.1 pg·mL–1, p=0.03).

In aggregate, these findings show that the initial phase of acute lung injury is associated with a decrease in vascular endothelial growth factor in the lung. This downregulation may represent a protective mechanism aimed at limiting endothelial permeability, and may participate in the decrease in capillary number that is observed during early acute respiratory distress syndrome.




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