Discussion: Environmental Factors

DR. WRIGHT: As a follow-up to my formal presentation, I would like to point out that the pathologists are quite aware of problems in diagnosing experimentally induced emphysema in an animal model. It would be nice to be able to perform the classical experiment, as exemplified in Pasteur's historical study of immunity to an-thrax in sheep, one in which a direct cause and effect can be demonstrated upon altering a single factor. Unfortunately, most of our experiments are not that straightforward. DR. GROSS: I think we are all in agreement with Dr. Kleinerman that destruction of alveolar walls is a sine qua non of emphysema. It seems to me that Dr. Pratt's criterion of emphysema-namely, the indispensable presence of unattached bands stretching across cystically enlarged air spaces-is based on an assumption. This assumption is that destruction of alveolar septa, when it occurs, is always incomplete so that bands remain. As seen from Dr. Kleinerman's presentation, there are areas of obvious emphysema where such bands are absent. Nevertheless, I agree that such apparently unattached bands seen in lung sections are indicative of alveolar destruction. However, I do not agree when Dr. Pratt insists that when these bands are absent , there is no alveolar destructon or emphysema. To produce emphysema our animals (guinea pigs, hamsters, and rats) are exposed to high concentrations of coal dust in an inhalation chamber. One half of the animals are given intratracheal injections of papain three months prior to the dust exposure. The dust is found collected within alveolar spaces, generally compactly aggregated. The alveolar walls are tightly contracted around dense dust masses. The contraction of the alveolar walls around the dust masses appears to sequester the dust and to cause the individual particles or macrophages to lose their identity while being compressed into masses that ultimately represent casts of the atelectatic alveoli. It seems highly probable that the mechanism of this sequestration is related to diffuse injury by the dust of the surfactant-secreting alveolar lining cells. The consequential increase in surface tension of the alveolar fluid film finally prevents the alveolus from expanding. Sections from a guinea pig given intratracheal papain and subsequently exposed to coal dust, reveal the sequestering atelectatic alveoli to be clustered about several alveolar ducts. The latter are dilated, but most of their evaginating alveoli are intact. In striking contrast, nonemphysematous tissue, with dust masses imprisoned in tightly contracted alveoli, is …