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Long‐term Differences in Lung Morphology in a Rat Model of Bronchopulmonary Dysplasia
Author(s) -
Shuster Taylor,
Haraldsdottir Kristin,
Kleinertz Aaron,
Eldridge Marlowe
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1017.6
Subject(s) - bronchopulmonary dysplasia , lung , term (time) , morphology (biology) , medicine , pathology , biology , zoology , physics , genetics , astronomy , pregnancy , gestational age
Bronchopulmonary dysplasia (BPD) is a chronic lung disease of prematurity associated with decreased alveolar and pulmonary vascular development that frequently results in the need for mechanical ventilation. The disease is a significant contributor to perinatal morbidity and mortality, and may lead to pulmonary hypertension (PH) and right ventricular hypertrophy during infancy. Although recent studies have shed light on the pathobiology of BPD, much remains unknown about the long‐lasting effects of the disease after adolescence. This research project had two primary aims. The first aim was to establish a working model of BPD and the second aim was to quantify the changes in alveolar number and density over time in healthy and diseased lungs. A rat model of BPD was created by exposing newborn Sprague Dawley rats to 85% O2 (BPD) for 14 days after birth. Controls (CTL) were exposed to 21% O2. Preliminary findings using H & E staining on lung sections and the mean linear intercept method indicate little recovery in alveolar septation between time points p7 and p14; we hypothesize further remodeling to occur over time the time points of p21, p28, p56, p90, and p180. This research adds further insight into possible alveolar remodeling that takes place in response to chronic lung disease, and will aid in predicting human responses to time and chronic lung disease.