GUINEA-PIG PULMONARY-HYPERTENSION CAUSED BY CIGARETTE-SMOKE CANNOT BEEXPLAINED BY CAPILLARY BED DESTRUCTION

Chronic exposure to cigarette smoke is known to produce pulmonary hype rtension in humans and in animal models, but the etiology of this proc ess is controversial. To evaluate whether alterations in the structure of the pulmonary capillary bed or the peribronchiolar arterioles coul d be correlated with the pulmonary arterial pressure (Ppa), we examine d the pulmonary vasculature in guinea pigs that had developed pulmonar y hypertension after being exposed to cigarette smoke for 6 mo. The sm oke-exposed animals had a significant increased Ppa compared with the control (air-exposed) animals (14.4 +/- 2.4 vs. 9.9 +/- 0.9 cmH(2)O). In the smoke-exposed animals, there was an increased percentage of mus cularized peribronchiolar arterioles (33.5 +/- 5.8% smoke exposed vs. 56.1 +/- 5.8% control), and the capillary diameter and density mere si gnificantly decreased in both the center and periphery of the lobule ( center diameter 8.8 +/- 1.9, periphery diameter 10.0 +/- 2.0 mu m, cen ter density 79 +/- 5, and periphery density 84 +/- 4 in smoked exposed vs. center diameter 7.7 +/- 1.9, periphery diameter 8.6 +/- 2.0 mu m, 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 produc es alteration of the capillary bed and pulmonary arterioles secondary to emphysematous air-space enlargement, these structural findings cann ot explain the increase in Ppa. It appears that pulmonary hypertension due to chronic cigarette smoke exposure is a result of a primary alte ration of capillary or muscular arteriolar vascular structure but inst ead may be secondary to alterations of the dynamic properties of the v ascular bed with subsequent increase in vascular resistance.