Kuhn C, Tavassoli F
Lab Invest. 1976 Jan;34(1):2-9.
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.
通过气管内单次注射25单位猪胰弹性蛋白酶在仓鼠中诱发肺气肿。在注射后24小时至1年的不同时间间隔,通过扫描电子显微镜检查肺部,并将其外观与人类肺气肿的实例进行比较。注射后24小时内,肺泡管扩张,气腔大小比正常情况更具变异性。气腔内存在纤维蛋白丝、红细胞和吞噬细胞。到一周时,出血和渗出物已消退,但在研究期间异常气腔持续扩大。异常气腔是由肺泡管逐渐扩张以及肺泡间隔缩短并偶尔消失形成的。肺泡孔偶尔扩大,但数量仅局部增加。人类先天性大叶性肺气肿和全小叶性肺气肿的单个实例外观与动物模型相似。异常气腔由扩张的肺泡管和肺泡间隔回缩形成。相比之下,在一些小叶中心性肺气肿病例中,肺泡间隔出现明显的开窗现象,大的气腔常常被一些先前存在的肺泡壁的丝状组织残余物穿过。结果表明,至少有两种形态发生过程导致肺气肿。一种是开窗融合导致肺泡壁破坏,另一种是通过仍有待确定的机制对肺结构进行逐渐重塑。