A light microscopic (LM), transmission electron microscopic (TEM), and scanning electron microscopic (SEM) study was performed on the lungs from seven baboons delivered by cesarean section prematurely (75% of full gestation) and one at full term. Six of the seven premature baboons pursued a clinical course typical of human hyaline membrane disease (HMD) and/or bronchopulmonary dysplasia (BPD). All the animals were supported with mechanical ventilation and exposed to continuous high levels of inspired oxygen. Three animals died early (≤3 days) of complications and two demonstrated typical light and electron microscopic lesions of hyaline membrane disease. Three baboons survived ≥ 8 days and developed pathologically confirmed bronchopulmonary dysplasia, characterized by an altered inflation pattern of atelectasis and overdistension/"emphysema," bronchial and bronchiolar lesions of necrosis, regenerative hyperplastic and/or squamous metaplastic changes, and peribronchiolar fibrosis and early alveolar wall fibrosis. A striking finding was a hyperplastic/obliterative respiratory bronchiolar lesion, most frequently seen in the atelectatic areas. The lungs of these animals lacked pores of Kohn; a feature shared by a study group of untreated baboons with gestation ages of 109 to 180 days. It is suggested that the lack of collateral ventilation, plus the striking hyperplastic-obliterative airway lesion might explain the characteristic feature of atelectasis. The histopathologic features of this model coincide with with those of BPD in the human neonate, with the exception of the hypertensive vascular changes, which may be a time-related lesion. The pathologic findings further support the premise that the premature baboon will be a very useful model in which the primary etiologic consideration of oxygen toxicity and barotrauma can be separated as to their roles in the causation of bronchopulmonary dysplasia.
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Molecular Biology
- Clinical Biochemistry