The scanning electron microscopy of elastase-induced emphysema. A comparison with emphysema in man.
Emphysema was produced in hamsters by a single intratracheal injection of 25 units of porcine pancreatic elastase. The lungs were examined by scanning electron microscopy at intervals from 24 hours to 1 year after the injection, and the appearance was compared to examples of human emphysema. Within 24 hours of injection, the alveolar ducts were dilated and air spaces were of more variable size than normal. Fibrin strands, erythrocytes and phagocytic cells were present in air spaces. By a week the hemorrhage and exudate had resolved, but adnormal air spaces continued to enlarge over the period of study. The abnormal airspaces formed by progressive dilation of alveolar ducts with shortening and occasionally effacement of interalveolar septa. Interalveolar pores were occasionally enlarged but only focally increased in number. The appearance of single examples of human congenital lobar emphysema and panlobular emphysema resembled the animal model. Abnormal air spaces were formed by dilated alveolar ducts with retraction of interalveolar septa. In contrast, in some cases of centrolobular emphysema marked fenestration of alveolar septa occurred and large air spaces were often traversed by threadlike strands of tissue remnants of some preexisting alveolar walls. The results suggest that there are at least two morphogenetic processes leading to emphysema. One is the coalescence of fenestrations leading to destruction of alveolar walls, and the other is a gradual remodeling of lung structure by mechanisms still to be defined.
D000328:Adult; D000818:Animals; D006224:Cricetinae; D006801:Humans; D007223:Infant; D008168:Lung / Q000473:pathology* / Q000648:ultrastructure; D008855:Microscopy, Electron, Scanning; D010196:Pancreatic Elastase; D011650:Pulmonary Alveoli / Q000473:pathology / Q000648:ultrastructure; D011656:Pulmonary Emphysema / Q000139:chemically induced / Q000473:pathology*; D013997:Time Factors
D010196:Pancreatic Elastase