Hayes J A, Korthy A, Snider G L
J Pathol. 1975 Sep;117(1):1-14. doi: 10.1002/path.1711170102.
A single dose of crystalline, porcine pancreatic elastase injected intratracheally into hamsters induces widespread alveolar enlargement with subpleural bullae. A uniformly severe lesion is consistently induced by 0-2 mg elastase per 100 g body weight and with negligible mortality. Compared with controls, which showed no lesion, elastase-damaged lungs show a highly significant (P less than or equal to 0-001) increase in alveolar size and a decrease in internal surface area. Taken with the associated physiological abnormalities, these findings closely simulate human emphysema of the panlobular (panacinar) type. Histologically it appears that elastase converts the fine elastic fibres in alveolar walls and pleura into thickened, nodular fibres which may also be broken along their length. With higher doses of elastase, i.e., 0-5 mg/100 g body weight, many pulmonary arteries showed segmental loss of inner and outer elastic laminae, usually with thrombosis on the overlying endothelium. The mechanism of this thrombosis is unclear. These experiments suggest that damage to elastic fibres may be an important element in the development of human panacinar emphysema, and that the damage could be one pathogenetic mechanism which produces damage of elastic fibres.
将单剂量的结晶猪胰弹性蛋白酶经气管内注入仓鼠体内，可导致广泛的肺泡扩大并伴有胸膜下大疱形成。每100克体重注射0 - 2毫克弹性蛋白酶可始终诱导出一致的严重病变，且死亡率可忽略不计。与无病变的对照组相比，弹性蛋白酶损伤的肺脏肺泡大小显著增加（P小于或等于0.001），内表面积减小。结合相关的生理异常情况，这些发现与人类全小叶（全腺泡）型肺气肿极为相似。组织学上，弹性蛋白酶似乎将肺泡壁和胸膜中的细弹性纤维转化为增厚的结节状纤维，这些纤维沿其长度方向也可能断裂。使用更高剂量的弹性蛋白酶，即每100克体重0 - 5毫克时，许多肺动脉显示出内外弹性膜的节段性缺失，通常在上覆内皮上伴有血栓形成。这种血栓形成的机制尚不清楚。这些实验表明，弹性纤维损伤可能是人类全腺泡型肺气肿发展中的一个重要因素，并且这种损伤可能是产生弹性纤维损伤的一种致病机制。
