Abstract

Whether meconium-stained amniotic fluid (MSAF) serves as an indicator of fetal distress is under debate; however, the presence of MSAF concerns both obstetricians and pediatricians because meconium aspiration is a major contributor to neonatal morbidity and mortality, even with appropriate treatment. The present study suggested that thick meconium in infants might be associated with poor outcomes compared with thin meconium based on chart reviews. In addition, cell survival assays following the incubation of various meconium concentrations with monolayers of human epithelial and embryonic lung fibroblast cell lines were consistent with the results obtained from chart reviews. Exposure to meconium resulted in the significant release of nitrite from A549 and HEL299 cells. Medicinal agents, including dexamethasone, L-Nω-nitro-arginine methylester (L-NAME), and NS-398 significantly reduced the meconium-induced release of nitrite. These results support the hypothesis that thick meconium is a risk factor for neonates who require resuscitation, and inflammation appears to serve as the primary mechanism for meconium-associated lung injury. A better understanding of the relationship between nitrite and inflammation could result in the development of promising treatments for meconium aspiration syndrome (MAS).

Highlights

  • Neonates were deemed to have suffered from meconium aspiration syndrome (MAS) and were admitted to the sick neonate care unit, and 12 neonates were admitted to the neonatal intensive care unit (NICU)

  • To investigate the effects of exposure to different meconium consistencies among infants diagnosed with MAS, we divided the infants diagnosed with MAS into thin and thick meconium groups, based on the data obtained from the chart review, resulting in 72 cases classified into the thin meconium group and 23 cases classified into the thick meconium group

  • The clinical features of MAS are characterized by profound functional alterations within the lung, associated with an intense inflammatory reaction, and thick meconium causes a more severe fetal inflammatory response than thin meconium

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Summary

Introduction

When the meconium becomes excreted into the amniotic cavity, meconium-stained amniotic fluid (MSAF) can be detected [6,7,8,9,10]. Animal studies showed that fetal swallowing was suppressed by hypoxia, leading to a decrease in the normal ability to clear meconium from the amniotic fluid [16]. Hypoxia may result in excessive meconium excretion, disturb clearance, and prolong MSAF, which is associated with intrauterine fetal death, low APGAR scores [17], intrapartum fetal death [18], neurologic impairments [19,20], and meconium aspiration syndrome (MAS) [21]

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