INTRODUCTION: Bronchopulmonary dysplasia (BPD) is a disease that is caused by prolonged high-concentration oxygen therapy, and its typical pathologic character is edema of pulmonary alveolus. Aquaporins play an important role in the fluid transition.
OBJECTIVE: The objective of this study was to examine the expression change of aquaporin 1 (AQP1) in hyperoxia-induced lung injury and the mechanism of action in lung edema.
METHODS: Thirty-two juvenile Wistar rats were randomly divided into breathing room air (n = 8) and hyperoxia exposure (O2 > 95%; n = 8 at 3, 7, and 14 days, respectively). The distribution of AQP1 in the lung tissues and its mRNA expressions were detected by immunohistochemistry and reverse-transcription polymerase chain reaction.
RESULTS: Light microscopic findings in the hyperoxia group included edema, hemorrhage, and extensive inflammatory cells. The lung wet/dry ratio, the protein content in bronchoalveolar lavage fluid, and the lung leak index in the hyperoxia group were significantly higher than those in room air group. The expression of AQP1 mRNA in the lungs was significantly decreased at 3 days of hyperoxia exposure, minimized at 7 days, and increased from 14 days. Immunohistochemistry for AQP1 was seen primarily in microvascular endothelia cells around bronchus and alveolus and interstitial cells; the positive regions were similar between the room air group and the hyperoxia group, AQP1 protein expression in the lungs was significantly decreased at 3 days of hyperoxia exposure, minimized at 7 days, but increased at 14 days. The dynamic changes of AQP1 protein level coincided with the changes of AQP1 mRNA expression.
CONCLUSIONS: Hyperoxic lung injury may induce regulative imbalance of aquaporin expression. It may be 1 of the reasons for lung edema caused by hyperoxic lung injury.
Submitted by Feng Xu
- Copyright © 2008 by the American Academy of Pediatrics