Progressive Vascular Functional and Structural Damage in a Bronchopulmonary Dysplasia Model in Preterm Rabbits Exposed to Hyperoxia

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dc.contributor.authorJiménez, Julio
dc.contributor.authorRichter, Jute
dc.contributor.authorNagatomo, Taro
dc.contributor.authorSalaets, Thomas
dc.contributor.authorQuarck, Rozzen
dc.contributor.authorWagennar, Allard
dc.contributor.authorWang, Hongmei
dc.contributor.authorVanoirbeek, Jeroen
dc.contributor.authorDeprest, Jan
dc.contributor.authorToelen, Jaan
dc.date.accessioned2021-12-14T20:43:47Z
dc.date.available2021-12-14T20:43:47Z
dc.date.issued2016
dc.description.abstractBronchopulmonary 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.es
dc.identifier.citationJiménez J, Richter J, Nagatomo T, Salaets T, Quarck R, Wagennar A, Wang H, Vanoirbeek J, Deprest J, Toelen J. Progressive Vascular Functional and Structural Damage in a Bronchopulmonary Dysplasia Model in Preterm Rabbits Exposed to Hyperoxia. Int J Mol Sci. 2016 Oct 24;17(10):1776.es
dc.identifier.urihttp://dx.doi.org/10.3390/ijms17101776es
dc.identifier.urihttp://hdl.handle.net/11447/5241
dc.language.isoen_USes
dc.subjectBronchopulmonary dysplasiaes
dc.subjectAnimal modelses
dc.subjectLung chronic diseasees
dc.subjectRabbit; lung functiones
dc.titleProgressive Vascular Functional and Structural Damage in a Bronchopulmonary Dysplasia Model in Preterm Rabbits Exposed to Hyperoxiaes
dc.typeArticlees

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