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Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T 2B5
Received 6 September 1996; accepted in final form 8 January 1997.
Yamato, H., J. P. Sun, A. Churg, and J. L. Wright.
Guinea pig pulmonary hypertension caused by cigarette smoke cannot be explained by capillary bed destruction. J. Appl.
Physiol. 82(5): 1644-1653, 1997.
Chronic exposure
to cigarette smoke is known to produce pulmonary hypertension in humans
and in animal models, but the etiology of this process is
controversial. To evaluate whether alterations in the structure of the
pulmonary capillary bed or the peribronchiolar arterioles could be
correlated with the pulmonary arterial pressure (Ppa), we examined the
pulmonary vasculature in guinea pigs that had developed pulmonary
hypertension after being exposed to cigarette smoke for 6 mo. The
smoke-exposed animals had a significant increased Ppa compared with the
control (air-exposed) animals (14.4 ± 2.4 vs. 9.9 ± 0.9 cmH2O). In the smoke-exposed
animals, there was an increased percentage of muscularized peribronchiolar arterioles (33.5 ± 5.8% smoke exposed vs. 56.1 ± 5.8% control), and the capillary diameter and density were
significantly decreased in both the center and periphery of the lobule
(center diameter 8.8 ± 1.9, periphery diameter 10.0 ± 2.0 µm,
center density 79 ± 5, and periphery density 84 ± 4 in smoked
exposed vs. center diameter 7.7 ± 1.9, periphery diameter 8.6 ± 2.0 µm, center density 73 ± 6, and periphery density 77 ± 6 in controls). Neither group showed any correlation between
these values and the Ppa. We conclude that although chronic exposure to
cigarette smoke produces alteration of the capillary bed and pulmonary
arterioles secondary to emphysematous air-space enlargement, these
structural findings cannot explain the increase in Ppa. It appears that
pulmonary hypertension due to chronic cigarette smoke exposure is a
result of a primary alteration of capillary or muscular arteriolar
vascular structure but instead may be secondary to alterations of the
dynamic properties of the vascular bed with subsequent increase in
vascular resistance.
emphysema
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