Background: Meconium aspiration-induced hypertensive lung injury is frequently associated with neuronal damage. Inhaled nitric oxide (iNO) is widely used in the treatment of pulmonary hypertension, but its effects on the brain are poorly known.
Aims: The aim of this study was to determine the effects of iNO treatment on the neuronal tissue after meconium aspiration.
Aim: Meconium aspiration-induced hypertensive lung injury, especially when connected with perinatal asphyxia, has been associated with brain damage. We aimed to determine the neuronal injury induced by pulmonary meconium contamination alone and with concurrent asphyxia.
Methods: 36 anaesthetized and ventilated newborn piglets were haemodynamically monitored for 6 h.
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.
Meconium aspiration and birth asphyxia are both separately connected to significant pulmonary and systemic hemodynamic changes in newborns, but, although these insults frequently coexist, their combined effects on the neonatal circulation are still controversial. To determine the pulmonary and systemic circulatory changes induced by pulmonary meconium contamination with concurrent asphyxia, 41 anesthetized and ventilated newborn piglets (10-12 d) were studied for 6 h. Eleven piglets were instilled with a bolus of human meconium intratracheally, and 10 piglets had meconium instillation with immediate induction of an asphyxic insult.
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