Barker (neonatal respiratory distress) syndrome in the pig: The ultrastructural pathology of the lung

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Abstract
The ultrastructural pathology of the lung of a naturally occurring, fatal respiratory distress syndrome of the newborn piglet is described. The pulmonary lesions are characterized by immaturity of the distal airways and of alveoli; by severe alveolar epithelial hyperplasia and hypertrophy; by increased width of the blood to air barrier; by alveolar and bronchiolar epithelial degeneration and separation; by the production of alveolar and bronchiolar hyaline membranes and by alveolar hemorrhage and alveolar and peribronchial edema. Many of the hyperplastic cells of the alveolar epithelium are pyramidal, rest on a basement membrane, have microvilli on their luminal surfaces, form tight junctions with their neighbors and contain reduced numbers of lamellated electron-dense inclusions in the cytoplasm. These cells are dystrophic type 2 pneumocytes. Other hyperplastic alveolar epithelial cells have some of these features and may be type 1 or type 2 pneumocytes. Both types contain large amounts of cytoplasmic carbohydrate material and are deficient in lamellated inclusions associated with type 2 pneumocytes of normal piglets. Increase in the thickness of the blood to air barrier from 0.22 .mu.m to 0.55 .mu.m in normal to 0.50 .mu.m to 2.33 .mu.m in moderately affected piglets, or to a maximum of 12 .mu.m in severely affected piglets, was associated with increasing respiratory distress. Hyaline membranes were composed of epithelial cellular debris from saccular and bronchiolar epithelium. The reduction in size and number of the specific lamellated cytoplasmic inclusions of type 2 pneumocytes in affected lungs was correlated with biochemical findings of increased surface tension and reduced phospholipid and lecithin contents of lung washings.