Diffuse Alveolar Damage in the Evolution of Bronchopulmonary Dysplasia in the Baboon

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Abstract
Pulmonary immaturity, oxygen exposure that elicits cellular damage by free radicals, and barotrauma induced by mechanical ventilation are implicated in the pathogenesis of bronchopulmonary dysplasia. In the adult counterpart of adult respiratory distress syndrome, diffuse alveolar damage characterizes a histopathological sequence of lung findings that can occur during the disease course. Although adult respiratory distress syndrome has many etiologies, elevated oxygen exposure is known to be a contributor to the ensuing lung injury. In bronchopulmonary dysplasia, oxygen exposure is thought to be a primary agent of injury. The evolution of the histopothological findings in the premature baboon model of hyaline membrane disease/bronchopulmonary dysplasia was investigated in this study and compared to that in oxygen-treated adult baboons with adult respiratory distress syndrome. Findings from lung specimens of 121 prematurely delivered baboons at 0, 0.5, 1, 2, 3–6, 7–11+ days after delivery document that the premature lung has a delayed and more blunted exudative response when compared to that of human and baboon adults. Saccular edema, not hyaline membranes, is the dominant histopathological finding in the exudative phase of diffuse alveolar damage and occurs later (7–11 days) in infant lungs when compared to comparably treated adult lungs in which maximal exudative changes are seen at 3–6 days. The reparative response in the premature baboon is characterized by saccular wall thickening and fibrosis, with less intramural organization of exudate in saccular/alveolar spaces when compared to adults. The airway changes in the premature are more severe than those seen in adult disease. These findings indicate that diffuse alveolar damage does occur in the immature lung albeit with differing characteristics when contrasted to comparably injured adults.