AJP - Lung Cellular and Molecular Physiology, Vol 267, Issue 5 557-L563, Copyright © 1994 by American Physiological Society
Cigarette smoke causes rapid cell proliferation in small airways and associated pulmonary arteries
H. S. Sekhon, J. L. Wright and A. Churg
Department of Pathology, University of British Columbia, Vancouver, Canada.
To determine whether smoke could directly affect the cells of the small
airways and the small vessels, we exposed Sprague-Dawley rats to the whole
smoke of 7 cigarettes/day for 1, 2, or 7 days. Three hours before the rats
were killed, 5-bromo-2'-deoxyuridine (BrdU) was administered. Labeled
nuclei were counted in histological sections stained with antibodies to
BrdU. In smokers, pulmonary artery walls at the level of the membranous
bronchioles (MB), respiratory bronchioles (RB), and alveolar ducts (AD)
showed significant increases in labeled nuclei at all three times;
increases in endothelial labeling were only present in vessels associated
with AD. Significantly increased labeling was also seen in the epithelium
and walls of MB and RB themselves at all time periods. However, there was
no correlation between labeling indexes in matched pairs of airways and
vessels. Smoke had no effect on the labeling of mesothelial and
submesothelial cells. We conclude that cigarette smoke rapidly causes
proliferation of intrinsic cells in the airways and small vessels; this
effect may lead eventually to airway wall muscular hyperplasia and fibrosis
(small airways disease) and to vascular changes associated with pulmonary
hypertension. However, the lack of correlation between labeling indexes in
the vessels and airways suggests that different mediators are involved at
these two sites. At least over the time course of this experiment, smoke
does not cause proliferation of mesothelial or submesothelial cells.
