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A Mouse Model of Cigarette Smoke-Induced Emphysema*

Kristen J. Nikula, DVM, PhD; Thomas H. March, DVM, PhD; J. Seagrave, PhD; G. Finch, PhD; E. Barr, MSEE; M. Ménache, PhD; F. Hahn, DVM; C. Hobbs, DVM
Author and Funding Information

*From the Lovelace Respiratory Research Institute, Albuquerque, NM. This research is supported by the Environmental Protection Agency, through the National Environmental Respiratory Center, and by the Assistant Secretary for Defense Programs, U.S. Department of Energy.

Correspondence to: Thomas H. March, DVM, PhD, Biopersistant Particle Center, Lovelace Respiratory Research Institute, P.O. Box 5890, Albuquerque, NM 87185



Chest. 2000;117(5_suppl_1):246S-247S. doi:10.1378/chest.117.5_suppl_1.246S
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Abbreviations: CS = cigarette smoke; Lm = mean linear intercepts of alveolar boundaries; Sva, pa = alveolar surface area per unit volume of lung parenchyma; Sa/Vair = alveolar surface area to volume parenchymal air; Vvsept = volume density of alveolar septa

Cigarette smoking is the major risk factor for pulmonary emphysema in humans. In this study, histopathology and stereology were used to assess emphysema in the lungs of female B6C3F1 mice exposed in whole-body chambers to either filtered air or cigarette smoke (CS) at a concentration of 250 mg total particulate material/m3 for 6 h/d, 5 d/wk, for either 7 or 13 months. Quantitative data obtained included the mean linear intercepts of alveolar boundaries (Lm, a measure of alveolar size), the volume density of alveolar septa (Vvsept), alveolar surface area per unit volume of lung parenchyma (Sva, pa), and the ratio of alveolar surface area to volume of parenchymal air (Sa/Vair). Morphologic evidence of tissue destruction in CS-exposed mice included enlarged alveoli that were irregular in size and shape and alveoli with multiple foci of septal discontinuities and isolated septal fragments. Compared with controls, CS-exposed mice had significantly greater lung volumes, larger alveoli (increased Lm), loss of alveolar septal tissue (decreased Vvsept), decreased density of alveolar surface (decreased Sva, pa), and decreased surface area relative to the volume of air (decreased Sa/Vair). Morphometric differences in the mice at 13 months were greater than they were at 7 months, suggesting progression of the disease. Gelatinase and elastolytic activities were greater in bronchoalveolar lavage fluid of comparison groups of mice exposed to CS for 30 months, compared with controls. The gelatinase activity was due to metalloproteinases and not cysteine or serine proteinases. The morphologic and stereologic data indicated that the alterations in CS-exposed mice met the definition of emphysema, ie, progressive dilation of airspaces distal to the terminal bronchioles, with destruction of alveolar septa.

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