Valentine R, Rucker R B, Chrisp C E, Fisher G L
Toxicol Appl Pharmacol. 1983 May;68(3):451-61. doi: 10.1016/0041-008x(83)90290-9.
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.
弹性蛋白酶诱导的肺气肿动物模型对于研究与肺气肿相关的生理、解剖和生化损伤可能是有用的。将猪胰弹性蛋白酶（每100克体重0.15或0.30毫克弹性蛋白酶）经气管内滴注到A/J品系小鼠体内后，检测了选定的肺损伤生化和形态学指标。弹性蛋白酶导致广泛的气腔扩大且死亡率不高。在2周内观察到终末细支气管远端肺实质的病变，其具有类似全小叶型和小叶中心型肺气肿的特征。肺气肿的形态学分析表明，在组织损伤和修复的急性期后，病变稳定，肺泡结构没有进一步恶化。气管内注入弹性蛋白酶后，肺弹性蛋白合成增加，治疗8周后肺弹性蛋白水平比对照组高30%。肺DNA和蛋白质水平的微小变化表明，弹性蛋白酶产生了不包括炎症和水肿的特定肺损伤。
