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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain
HIGHER OXYGEN CONCENTRATIONS AT BIRTH ENHANCE LUNG INFLAMMATION AND CHRONIC LUNG DISEASE IN THE EXTREMELY PREMATURE INFANT
Abstract number: P12
Brugada M, Aguar M, Escrig R, Escobar J, Arduini A, Sastre J, Izquierdo I, Gimeno A, Saenz P, Ledo A, Vento M
Neonatal Division; University Hospital La Fe; 46009 Valencia; Spain.
Physiology Dpt; Faculty of Pharmacy; 46100 Burjassot; Valencia; Spain. [email protected]
Background:
Extremely low birth weight infants (ELBW) have an immature lung in the saccular phase of development. After birth they need active resuscitation with positive pressure ventilation (PPV). Lung stretch causes pathophysiological alterations leading to lung inflammation (1). However, oxygen supplementation could be an additional factor leading to chronic lung disease (CLD).
Aim:
(1) Evaluate pro-inflammatory cytokines in ELBW receiving positive pressure ventilation (PPV) and 2 different [O2] in the delivery room (DR). (2) Establish a correlation between O2 supplementation in the DR and development of CLD.
Material & Methods:
IL8 and TNF 1a were determined in cord blood and at day 1 and weeks 2, 3 and 5 in ELBW infants resuscitated with PPV and 30% or 90% O2 at birth. Pro-inflammatory cytokines were determined by cytometric bead array.
Results:
IL8 was significantly higher in ventilated babies that additionally received higher oxygen supplementation along the study. Although TNF 1a was also increased comparatively in the higher oxygen group, differences were only significant in the first 2 weeks of life, and not thereafter. There was a positive correlation between IL8 and TNF 1a in the first 2 weeks of like and later development of chronic lung disease.
Conclusions:
Lung stretching has been shown to enhance lung inflammation (1) but additionally the use of higher oxygen concentrations upon resuscitation worsens this tendency and prompts development of chronic lung disease.
References:
Hillman N et al Am J Respir Crit Care Med 2007.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :P12