Wright J L, Ngai T, Churg A
Department of Pathology, University of British Columbia, Vancouver, Canada.
Exp Lung Res. 1992 Jan-Mar;18(1):105-14. doi: 10.3109/01902149209020654.
Smoke-induced airway abnormalities are a common feature of the lungs of cigarette smokers. We examined the small airways from guinea pigs exposed to cigarette smoke for periods of 1, 3, 6, and 12 months, and compared these data to those obtained from age-matched, nonexposed animals. We found that there was no change in the structure of the airway walls, and that similar numbers of peribronchiolar alveolar attachments were present in both groups. However, the airway epithelium of animals exposed to smoke for 3, 6, and 12 months had greater numbers of secretory cells/mm length basement membrane. We conclude that this guinea pig model of cigarette smoke-induced lung disease mimics the human condition in that there is alteration of the cellular population of the small airway epithelium. However, the lack of structural changes in the airway wall, with no evidence of peribronchiolar alveolar destruction, suggests that the airflow obstruction seen in these animals is most likely due to emphysematous parenchymal destruction with loss of elastic recoil.
烟雾诱导的气道异常是吸烟者肺部的常见特征。我们检查了暴露于香烟烟雾1个月、3个月、6个月和12个月的豚鼠的小气道，并将这些数据与从年龄匹配的未暴露动物获得的数据进行比较。我们发现气道壁结构没有变化，两组中支气管周围肺泡附着的数量相似。然而，暴露于烟雾3个月、6个月和12个月的动物的气道上皮每毫米基底膜长度有更多的分泌细胞。我们得出结论，这种香烟烟雾诱导的肺部疾病豚鼠模型模拟了人类情况，即小气道上皮细胞群体发生了改变。然而，气道壁缺乏结构变化，没有支气管周围肺泡破坏的证据，这表明这些动物中出现的气流阻塞很可能是由于肺气肿实质破坏和弹性回缩丧失所致。
