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CURATOR

PhD Student, Monash University, Central Clinical Schools

PINBOARD SUMMARY

Exploring the link between two neonatal disorders that arise as a complication of supplemental O2.

Bronchopulmonary dyplasia (BPD) and retinopathy of prematurity (ROP) are two major disorders of preterm birth and arise as a complication of exposure to supplemental oxygen given to treat breathing difficulties in these babies. Approximately 68-75% of premature infants weighing less than 1500g are diagnosed with BPD and ROP which often progress into severe lung disease known as Chronic Obstructive Pulmonary Disease (COPD), the world’s third leading cause of death or vision loss in the eye. Previously BPD and ROP were viewed as two distinct disorders even though they often occur simultaneously in a single infant. There are presently no cures for these conditions and only limited treatment options are available. Therefore, we hypothesise that there is an underlying mechanism that links the two disorders together. By modelling BPD and ROP disease progression together we will be able to better understand the pathways that lead to the development of these disorders, in order to find an effective preventative treatment for BPD and ROP.

3 ITEMS PINNED

Impact of bronchopulmonary dysplasia on brain and retina.

Abstract: Many premature newborns develop bronchopulmonary dysplasia (BPD), a chronic lung disease resulting from prolonged mechanical ventilation and hyperoxia. BPD survivors typically suffer long-term injuries not only to the lungs, but also to the brain and retina. However, currently it is not clear whether the brain and retinal injuries in these newborns are related only to their prematurity, or also to BPD. We investigated whether the hyperoxia known to cause histologic changes in the lungs similar to BPD in an animal model also causes brain and retinal injuries. Sprague Dawley rat pups were exposed to hyperoxia (95% O2, 'BPD' group) or room air (21% O2, 'control' group) from postnatal day 4-14 (P4-14); the rat pups were housed in room air between P14 and P28. At P28, they were sacrificed, and their lungs, brain, and eyes were extracted. Hematoxylin and eosin staining was performed on lung and brain sections; retinas were stained with Toluidine Blue. Hyperoxia exposure resulted in an increased mean linear intercept in the lungs (P<0.0001). This increase was associated with a decrease in some brain structures [especially the whole-brain surface (P=0.02)], as well as a decrease in the thickness of the retinal layers [especially the total retina (P=0.0008)], compared to the room air control group. In addition, a significant negative relationship was observed between the lung structures and the brain (r=-0.49,P=0.02) and retina (r=-0.70,P=0.0008) structures. In conclusion, hyperoxia exposure impaired lung, brain, and retina structures. More severe lung injuries correlated with more severe brain and retinal injuries. This result suggests that the same animal model of chronic neonatal hyperoxia can be used to simultaneously study lung, brain and retinal injuries related to hyperoxia.

Pub.: 19 Mar '16, Pinned: 28 Aug '17