The morphologic basis for airflow obstruction in chronic obstructive pulmonary disease is extremely complex and consists of heterogeneous lesions. Emphysema seems to be the single most important lesion in this disorder. Abnormalities of the peripheral conducting airways, including inflammation, fibrosis, smooth muscle hypertrophy, and hyperplasia of mucussecreting elements, are also of functional importance. Low-grade inflammation involving both airways and parenchyma occurs after only short-term exposure to cigarette smoke. This chronic inflammatory reaction may initiate other, largely irreversible, tissue responses that are responsible for airflow function. In the case of emphysema, tissue obstruction is thought to be due to an elastase-antielastase imbalance, leading to accelerated destruction of elastic fibers in the alveolar walls. Logical strategies for controlling the development of emphysema might include measures to prevent the influx of phagocyte-borne elastases into the lung as well as efforts to supplement the antiprotease shield of the lower airways. Antiinflammatory drugs might also be effective in suppressing cigarette-smoke-induced reactions in the conducting airways. Other agents might be effective by preventing bronchoconstriction and the proliferation of smooth muscle elements in airway walls.
|Original language||English (US)|
|Journal||The American journal of medicine|
|Issue number||4 SUPPL. 1|
|State||Published - Oct 21 1991|
PubMed: MeSH publication types
- Journal Article