Background: 

Fetal to neonatal transition implies a brisk increment in arterial oxygen saturation which causes oxidative stress (1). The use of high oxygen concentrations especially in extremely premature infants may cause lung damage and inflammation contributing to the development of chronic lung disease.

Aim: 

To prove if higher versus lower oxygen concentration for resuscitation of extremely premature neonates causes increased expression of oxidative stress markers.

Methods: 

Prospective randomized trial enrolling neonates <= 28 weeks resuscitated with 30% (Lox) or 90% (Hox) oxygen at birth. GSH, GSSG were determined in cord blood, at day 1 & 3 by HPLC. O-tyrosine/phenylalanine and 8-oxo-2de-oxiguanosine/2de-oxiguanosine (by HPLC coupled to MS/MS) and F2-isoprostanes and Isofurans (by GC coupled to MS/MS) performed in urine at day 1 & 7. Follow-up until discharge.

Results: 

GSSG/GSH was higher in Hox on d1 (p<0.01) and 3 (p<0.01).Isofurans, O-tyr/Phenyl and 8oxodG/2dG in Hox were significantly higher on d1 (p<0.01) & d7 (p<0.05). A significant correlation between these parameters and development of chronic lung disease was established (figure).

Conclusions: 

(1) Brief exposure to high [O₂] of immature lung causes oxidative stress which is linked to CLD. (2) Non-invasive markers of oxidative stress are valuable predictors and useful for clinical purposes.

References: 

Vento M et al. Am J Respir Crit Care Med 2005.