Role of Meconium and Hypoxia in Meconium Aspiration-Induced Lung Injury in Neonatal Rabbits

• Main Authors: Alex Zagariya, Monica Sierzputovska, Shan Navale, Dharmapuri Vidyasagar
• Format: Article
• Language: English
• Published: Hindawi Limited 2010-01-01
• Series: Mediators of Inflammation
• Online Access: http://dx.doi.org/10.1155/2010/204831
• ISSN: 0962-9351; 1466-1861

Background. We previously showed that meconium cuases 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% O2), and (V) 5 minutes of hypoxia (95% O2). 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 maily from meconium itself.