Presented at the Neonatal Society 2004 Spring Meeting.
Gottstein R, Peake M, Bates M, Vince G, Subhedar NV
Neonatal Intensive Care Unit, Liverpool Women’s Hospital
Background: Arrested airway and vascular development is a characteristic pathological finding in preterm infants dying with CLD. Vascular Endothelial Growth Factor (VEGF) is an endothelial specific mitogen which is important in physiological and pathological angiogenesis. Some studies have suggested that VEGF concentrations in bronchoalveolar lavage fluid (BALF) are decreased during the first week of life in infants who subsequently develop CLD (1). Levels of soluble VEGF receptors 1 and 2 (sVEGFR-1, sVEGFR-2), naturally occurring inhibitors of VEGF activity, have not been reported previously in neonates.
Aims : The aims of this study were to measure plasma and BALF concentrations of VEGF, sVEGFR-1 and sVEGFR-2 in preterm infants < 32 weeks gestation, and to compare levels in infants with established CLD with preterm controls.
Methods : Three groups were studied: Group 1 (CLD group) comprised preterm infants with established CLD ventilated at 28 days of age; Group 2 (control group) were ventilated preterm infants < 7 days of age; Group 3 (control group) were healthy non-ventilated preterm infants at 28 days of age. BALF and/or plasma samples were taken and VEGF, and sVEGFR-1 and sVEGFR-2 concentrations measured using an ELISA technique (Quantikine, R&D systems).
Conclusions : VEGF, sVEGFR-1 and sVEGFR-2 were measurable in both BALF and plasma from preterm infants. VEGF and sVEGFR-1 concentrations were several times higher in BALF compared to plasma suggesting local synthesis of VEGF and sVEGFR-1 in the preterm lung. Infants with established CLD tended to have higher plasma and BALF VEGF, but lower sVEGFR-1 levels, compared to ventilated control infants < 7 days. VEGF and sVEGFR-1 may play a role in preterm lung injury.
References
1. Lassus P, Ristimaki A, Ylikorkala O, Viinikka L, Andersson S. Vascular endothelial growth factor in human preterm lung. Am J Respir Crit Care Med 1999;159:1429-33