Morphological and biochemical features of elastase-induced emphysema in strain A/J mice.
Elastase-induced animal models of pulmonary emphysema are potentially useful to study the physiological, anatomical, and biochemical injuries associated with emphysema. After the endotracheal instillation of porcine pancreatic elastase (0.15 or 0.30 mg elastase per 100 g body weight) into strain A/J mice, selected biochemical and morphometric indices od lung damage were examined. Elastase produced extensive air space enlargement without appreciable mortality. Lesions involving the lung parenchyma distal to the terminal bronchioles were observed within 2 weeks and possessed features resembling panlobular and centrilobular emphysema. Morphometric analyses of emphysema indicated that after the acute phase of tissue damage and repair, the lesions stabilize without further deterioration of alveolar structure. Increased lung elastin synthesis was noted following endotracheal elastase, resulting in lung elastin levels 30% higher than controls 8 weeks after treatment. Minimal alterations to lung DNA and protein levels indicated that elastase produced specific lung lesions exclusive of inflammation and edema.
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D008168:Lung / Q000473:pathology*; D051379:Mice; D008805:Mice, Inbred A; D009929:Organ Size / Q000187:drug effects; D010196:Pancreatic Elastase / Q000494:pharmacology*; D011656:Pulmonary Emphysema / Q000139:chemically induced* / Q000473:pathology
D010196:Pancreatic Elastase