Objectives: 

Aspirated meconium harms newborn pulmonary tissue on multiple levels. In addition to mechanical obstruction and surfactant inactivation, the presence of meconium induces transcription of pro-oxidative mediators which cooperate in pathogenesis of inflammatory changes and may negatively affect the common used therapy. However, inflammation is not treated on the present nor the time dependence of oxidative damage is known.The aim of our study was to describe time course of oxidative stress markers production during meconium aspiration syndrome (MAS).

Materials: 

New Zealand white rabbits were instilled by saline or meconium suspension and ventilated for 5 hours. Blood samples were taken before meconium application and in time intervals 1, 3 and 5 hours after application for evaluating of secondary products of oxidative stress (thiobarbituric acid reactive substances (TBARS) and 3-nitrotyrosine (3NT)) and differential white cell count. Oxidative damage and leukocyte differential were asessed also in lung tissue and bronchoalveolar lavage fluid (BALF) post mortem. Statistical analysis was applied using ANOVA and non-parametric tests.

Results: 

No change in oxidative markers production was seen after saline instillation although there was a transient decrease in leukocyte count. A decrease in leukocytes was found already in the first hour after meconium instillation and persisted till the end of experiment. Massive influx of neutrophils into lungs was manifested by higher neutrophil count in BALF. 3NT production in meconium group culminated in the 1st hour, while TBARS in the 3rd hour. Time changes in 3NT levels, but not TBARS levels, correlated negatively with changes in leukocyte count.

Conclusions: 

We suggest that the first hour after meconium aspiration is a crucial period for neutrophil-dependent oxidative damage development, however, it seems that another prooxidative cascades are activated which can later affect the therapy of MAS. Supported by: CEPV II 26220120036; VEGA 1/0291/12; Grant UK 461/2012.