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

Mediators Inflamm

Neonatology Research Laboratories, Department of Pediatrics, Michael Reese Hospital, Chicago, IL 60616, USA.

Published: April 2011

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3018642PMC
http://dx.doi.org/10.1155/2010/204831DOI Listing

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