COLLAGEN CONTENT OF ALVEOLAR WALL TISSUE IN EMPHYSEMATOUS AND NON-EMPHYSEMATOUS LUNGS

Background - Emphysema is currently defined as ''a condition of the lu ng characterised by abnormal, permanent enlargement of the airspaces d istal to the terminal bronchiole, accompanied by destruction of their walls, and without obvious fibrosis.'' The functional and morphologica l changes that occur in emphysema have largely been attributed to chan ges in alveolar elastin rather than in collagen. A study was performed to determine whether the amount of collagen in the alveolar wall chan ges with age in the lungs of non-smokers and of smokers with different types of macroscopically defined emphysema in relation to a microscop ic measurement of lung structure. Methods - Total alveolar wall collag en was measured (as hydroxyproline) in known volumes of distended lung tissue (by reverse phase high pressure liquid chromatography) in the lungs of nonsmokers (n = 23) and in regions sampled away from emphysem atous lesions in the lungs of 36 smokers (four with no emphysema, 13 w ith centriacinar emphysema (CAE), nine with panacinar emphysema (PAE), and 10 with a mixture (MIX) of both PAE and CAE). Mean lung airspace wall surface area per unit volume (AWUV) was calculated from at least six random blocks per lung and on histological sections immediately ad jacent to those prepared for collagen measurement with a rapid scannin g device (fast interval processor). Results - In non-smokers there was no significant correlation between the amount of collagen in the alve olar wall tissue and either mean lung AWUV or increasing patient age w hen amounts of collagen were expressed either per unit volume of diste nded lung (40 mm(3) sample) or per unit surface area of airspace wall tissue. Smokers without emphysema had similar amounts of collagen to n on-smokers. Lungs with PAE and MIX, but not CAE alone, contained signi ficantly more collagen than normal when expressed per unit volume of a irspace wall tissue whereas all groups, including CAE, contained signi ficantly raised amounts of collagen when expressed per unit surface ar ea. Conclusions - There is no significant age related change in the co llagen content of the lungs of non-smokers which suggests that, as AWU V is lost with age, the main collagenous framework is maintained. Howe ver, in smokers with emphysema there is a loss of airspace wall tissue in regions remote from the macroscopic lesions that is accompanied by a net increase in collagen mass. The greater accumulation of collagen in MIX lungs than in CAE lungs suggests a greater degree of structura l damage, indicative of an alternative pathogenetic mechanism operatin g between the different types of emphysema. Our results suggest an act ive alveolar wall fibrosis in emphysema as a consequence of cigarette smoking. It is suggested that the definition of emphysema may require further revision to include such change.