Author(s): Aaltonen M, Soukka H, Halkola L, Jalonen J, Holopainen IE,
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Abstract BACKGROUND: Meconium aspiration-induced hypertensive lung injury has been associated with neuronal damage in the newborn, but the mechanisms of the injury are poorly known. AIMS: The aim of the study was to determine the contribution of oxidative stress to the brain damage after pulmonary meconium contamination. STUDY DESIGN: Sixteen anesthetized and ventilated newborn piglets were studied for 6 h. Eight piglets were instilled with a bolus of human meconium intratracheally and eight piglets with saline instillation served as controls. Brain tissue lipid peroxidation products (TBARS), reduced glutathione (GSH), myeloperoxidase activity and oxidized DNA were analyzed as indicators of oxidative stress. RESULTS: Meconium aspiration did not change the systemic or carotid hemodynamics, but caused a well-established pulmonary hypertensive response. Sustained increase in additional oxygen demand was also observed after meconium insult, but no actual hypoxemia or hypercarbia was evident during the whole study period. Myeloperoxidase activity was elevated in the cerebellum after pulmonary meconium instillation, whereas concentrations of peroxidation products and glutathione were similar in the cortical, cerebellar and hippocampal regions of the two groups. Still, the amount of oxidized DNA was increased in the hippocampus of the meconium-aspirated piglets when compared to controls. CONCLUSIONS: Our data thus suggest that oxidative injury associated with pulmonary, but not systemic, hemodynamic disturbances may contribute to hippocampal damage after meconium aspiration in newborns.
This article was published in Early Hum Dev
and referenced in Journal of Clinical & Experimental Pharmacology