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Mediators Inflamm. 2010;2010:204831. doi: 10.1155/2010/204831. Epub 2010 Dec 30.

Role of meconium and hypoxia in meconium aspiration-induced lung injury in neonatal rabbits.

Author information

1
Neonatology Research Laboratories, Department of Pediatrics, Michael Reese Hospital, Chicago, IL 60616, USA. zagariya@uic.edu

Abstract

BACKGROUND:

We previously showed that meconium causes lung cell death by apoptosis and inflammatory cytokine expression. Whether this is due to meconium exposure itself, or meconium related hypoxia remains unclear.

OBJECTIVES:

To elucidate the effects of meconium, saline, milk, hypoxia and hyperoxia induced lung injury.

DESIGN/METHODS:

We studied 5 groups of rabbit pups: (I) normal saline; (II) Milk; (III) 10% solution of meconium; (IV) only to 15 minutes of hypoxia (10% O(2)), and (V) 5 minutes of hypoxia (95% O(2)). After exposure lung lavage cells were used for apoptotic cell count and cytokine expression. In vitro response of human A 549 epithelial cells to meconium-and milk exposure was also studied.

RESULTS:

There was no difference in cell death between saline and milk groups. However, meconium caused a significant cell loss compared to saline and milk-Inflammatory cytokines increased significantly in meconium group compared to saline or milk group. Although hypoxic and hyperoxic lungs showed increased inflammatory reaction compared to saline-treated lungs, this injury was not significant compared to meconium group. Studies with A549 cells also showed similar results.

CONCLUSIONS:

We conclude that lung cell injury in meconium aspiration is mainly from meconium itself.

PMID:
21234319
PMCID:
PMC3018642
DOI:
10.1155/2010/204831
[Indexed for MEDLINE]
Free PMC Article

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