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Abstract
Bronchopulmonary dysplasia (BPD) is caused by preterm neonatal lung injury and results in oxygen dependency and pulmonary hypertension. Current clinical management fails to reduce the incidence of BPD, which calls for novel therapies. Fetal rabbits have a lung development that mimics humans and can be used as a translational model to test novel treatment options. In preterm rabbits, exposure to hyperoxia leads to parenchymal changes, yet vascular damage has not been studied in this model. In this study we document the early functional and structural changes of the lung vasculature in preterm rabbits that are induced by hyperoxia after birth. Pulmonary artery Doppler measurements, micro-CT barium angiograms and media thickness of peripheral pulmonary arteries were affected after seven days of hyperoxia when compared to controls. The parenchyma was also affected both at the functional and structural level. Lung function testing showed higher tissue resistance and elastance, with a decreased lung compliance and lung capacity. Histologically hyperoxia leads to fewer and larger alveoli with thicker walls, less developed distal airways and more inflammation than normoxia. In conclusion, we show that the rabbit model develops pulmonary hypertension and developmental lung arrest after preterm lung injury, which parallel the early changes in human BPD. Thus it enables the testing of pharmaceutical agents that target the cardiovascular compartment of the lung for further translation towards the clinic.
Highlights
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that represents one of the most important diseases of preterm birth survivors [1]
BPD is characterized by an arrested lung development, vascular changes and inflammation [3,4]
Infants with BPD are at risk for recurrent and prolonged hospitalizations, higher complications of other pathologies related with prematurity, and lifelong alterations in lung function [1]
Summary
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that represents one of the most important diseases of preterm birth survivors [1]. Like sheep or non-human primates, are better mimics of fetal and postnatal lung development, but their use entails higher costs and housing demands, and their gestation lasts longer, with only one or two fetuses per pregnancy In all these models, vascular damage has been characterized [10,12,13,14]. Rabbits combine elements of the rodent and larger animal models, as they have a relatively short pregnancy duration and a large litter size [11] and display comparable perinatal lung development to humans Their lungs show comparable histological changes and inflammatory responses when exposed to hyperoxia, including alveolar simplification and lung function impairment [15]. This will strengthen the value of the rabbit model both in the study of the physiology and in the testing of experimental therapies before translation towards larger animal models
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