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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care

Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
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Minerva Anestesiologica 2010 August;76(8):609-16


language: English

Vascular endothelial growth factor: a possible mediator of endothelial activation in acute respiratory distress syndrome

Azamfirei L. 1, Gurzu S. 2, Solomon R. 3, Copotoiu R. 1, Copotoiu S. 1, Jung I. 2, Tilinca M. 4, Branzaniuc K. 5, Corneci D. 6, Szederjesi J. 1, Kovacs J. 1

1 Department of Intensive Care, University of Medicine and Pharmacy, Targu-Mures, Romania; 2 Department of Pathology, University of Medicine and Pharmacy, Targu-Mures, Romania; 3 Department of Intensive Care, University Hospital, Targu-Mures, Romania; 4 Department of Cell Biology, University of Medicine and Pharmacy, Targu-Mures, Romania; 5 Department of Anatomy and Embryology, University of Medicine and Pharmacy, Targu-Mures, Romania; 6 Department of Intensive Care, University of Medicine and Pharmacy Carol Davila Bucharest, Romania


AIM: Vascular endothelial growth factor (VEGF) is a potent angiogenic and endothelial factor, which is abundantly found in the normal lung tissue. The objective of the study was to assess the VEGF levels in lung tissue and plasma in acute respiratory distress syndrome (ARDS) patients compared with controls who died from non-ARDS causes.
METHODS: Plasma and tissue samples were prospectively collected from 20 patients with ARDS within 6 hours after intubation (VEGF in plasma and tissue samples) and on the day of extubation (plasma VEGF) or postmortem (lung tissue). We used an ELISA to measure the VEGF level in plasma. Lung specimens were obtained by bronchoscopic biopsy or by open biopsy during autopsy. All lung samples were stained for standard histopathological analysis and for immunohistochemical methods. Biomarker levels were compared between survivors (N=12), non-survivors (N=8) and controls (N=10).
RESULTS: Compared with the levels in controls, in the early stages of ARDS, plasma VEGF levels rose and intrapulmonary levels fell, but during recovery, these levels went back to normal levels.
CONCLUSION: The initial phase of ARDS is associated with a decrease in VEGF in the lung and an increase in the plasma. This down-regulation may represent a protective mechanism aimed at limiting endothelial permeability and may participate in the decrease in the capillary number that is observed during early ARDS. A persistent elevation of plasma VEGF over time predicts poor outcome.

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