Meconium aspiration syndrome (MAS) - Where do we go? Research perspectives.

The pathogenetic cascade of meconium aspiration syndrome (MAS) in newborn infants is complex and still incompletely studied. The variable clinical presentation of MAS is basically connected with variation of the amount and consistency of aspirated meconium and also its distribution within the affected lungs. The contributing role of other factors, like intrauterine fetal compromises, lung maturity at the time of insult as well as direct and indirect effects of meconium and its components on the lung alveolar and vascular integrity and development, remains to be studied in further detail.

Inhaled nitric oxide treatment inhibits neuronal injury after meconium aspiration in piglets.

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.

Meconium aspiration induces neuronal injury in piglets.

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.

Meconium aspiration induces oxidative injury in the hippocampus of newborn piglets.

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.

Angiotensin II receptor inhibition prevents pneumocyte apoptosis in surfactant-depleted rat lungs.

Pneumocyte apoptosis is implicated in the pathophysiology of acute inflammatory lung injuries in newborns and adults. Pulmonary angiotensin (ANG) II contributes to lung epithelial apoptosis in vitro, but its role in acute lung injury in vivo is unclear. We therefore studied the effects of ANG II receptor action on the pulmonary inflammatory and apoptotic changes in surfactant-depleted lungs in rats.

Meconium induces only localized inflammatory lung injury in piglets.

Neonatal meconium aspiration often produces severe respiratory distress due to an inflammatory pulmonary injury, but the extension of this damaging reaction to the noncontaminated lung regions is still uncertain. To investigate the presence of generalized pulmonary inflammatory response, 31 anesthetized and ventilated neonatal piglets (1-3 d) were studied. Meconium (n = 16) or saline (n = 15) was instilled unilaterally into the right lung, and analysis of the lung tissue or bronchoalveolar lavage (BAL) fluid from both lungs was performed after 12 h.

Asphyxia aggravates systemic hypotension but not pulmonary hypertension in piglets with meconium aspiration.

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.

Lung epithelial cells undergo apoptosis in neonatal respiratory distress syndrome.

For studying the presence of programmed cell death in the lungs of infants with fatal respiratory distress syndrome (RDS) and the possible contribution of postnatal glucocorticoid administration on this cell destruction, lung tissue samples from autopsies of 16 premature infants with fatal RDS were studied. The infants had neither been exposed to antenatal steroids nor received surfactant therapy, but seven of these infants had been subjected to postnatal dexamethasone treatment. Lung autopsy samples of seven term and two preterm neonates without any obvious lung disease served as controls.

Meconium stimulates neutrophil oxidative burst.

Acute lung injury induced by meconium aspiration is characterized by rapidly developing pulmonary inflammation with influx of activated polymorphonuclear cells. To evaluate the role of meconium in the activation of these invading cells, we described the oxidative capacity of circulating neutrophils after intratracheal administration of thick human meconium in pigs. We also examined the direct effects of varying meconium concentrations on the oxidative burst of human neutrophils in vitro.