Guinea pig pulmonary hypertension caused by cigarette smoke cannot be explained by capillary bed destruction.

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 microns, 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 microns, 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.