Critical Care

, 13:P54 | Cite as

Decreased vascular endothelial growth factor expression in lung tissue during acute respiratory distress syndrome

  • L Azamfirei
  • S Gurzu
  • S Copotoiu
  • I Jung
  • R Copotoiu
  • K Branzaniuc
  • R Solomon
Poster presentation

Keywords

Vascular Endothelial Growth Factor Lung Tissue Alveolar Macrophage Acute Respiratory Distress Syndrome Vascular Endothelial Growth Factor Expression 

Introduction

Endothelial injury is an important prognostic factor in acute respiratory distress syndrome (ARDS) [1, 2]. Vascular endothelial growth factor (VEGF) plays a critical role in endothelial destruction and angiogenesis [3]. The expression of VEGF in ARDS varies, depending on epithelial and endothelial damage [4, 5]. The objective of this study was to investigate the expression of VEGF in lung tissue from ARDS patients.

Methods

Lung specimens were obtained by autopsy from 10 patients with severe ARDS and were compared with a control group of 10 non-ARDS patients autopsied. All lung samples were stained for standard histopathological analysis and for immunohistochemical methods using a specific mouse monoclonal antibody.

Results

Compared with expression in non-ARDS control individuals, pulmonary expression of VEGF was significantly decreased (P < 0.001) in ARDS patients. Alveolar macrophages were similarly immunopositive in both groups. No differences were noted with regard to the individual patient's characteristics (age, gender, period of ARDS condition, number of ICU days).

Conclusion

A decrease in alveolar type II cellularity, due to apoptosis, has been observed during ARDS that may reduce the production of VEGF in the alveolar space and may participate in the decrease in lung perfusion.

Notes

Acknowledgements

Research Grant No. 136/IDEI from the National Authority of Scientific Research, Romania.

References

  1. 1.
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    Gerber HP, Wu X, Yu L, Wiesmann C, et al.: Mice expressing a humanized form of VEGF-A may provide insights into the safety and efficacy of anti-VEGF antibodies. Proc Natl Acad Sci USA 2007, 104: 3478-3483. 10.1073/pnas.0611492104CrossRefGoogle Scholar
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Copyright information

© Azamfirei et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

Authors and Affiliations

  • L Azamfirei
    • 1
  • S Gurzu
    • 1
  • S Copotoiu
    • 1
  • I Jung
    • 1
  • R Copotoiu
    • 1
  • K Branzaniuc
    • 1
  • R Solomon
    • 1
  1. 1.University of Medicine and PharmacyTargu MuresRomania

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