Dissociation of chronic vascular cell proliferation and vascular contractility after chronic cigarette smoke exposure

In guinea pigs, chronic cigarette smoke exposure produces physiological and structural alterations in the pulmonary vasculature Fia unknown mechanisms . This study. aimed to determine whether chronic cigarette smoke exposure c an induce altered pulmonary vascular reactivity, and whether chronic smoke exposure would be associated with a continued increase in vascular cell deo xyribonucleic acid (DNA) synthesis, indicative of cell proliferation. Guine a-pigs were therefore exposed to two regimens of smoke. In the first experiment, animals were exposed once to the smoke of seven ci garettes, and sacrificed 24 h post-smoke, while in the second experiment, t he guinea-pigs sere exposed for 5 days each week for 4 months. Control anim als were exposed to air. tung explant preparations and computer Linked imag e photography were utilized to determine vascular reactivity; and DNA synth esis was assessed using the 5-bromo-2'-deoxyuridine technique. Neither acute nor chronic smoke exposure affected vascular reactivity, alth ough the older animals had lesser reactivity. In the chronically smoked ani mals, evidence was found of ongoing vascular DNA synthesis, and evidence of structural alterations with increased muscularization of the arterioles (3 4.7+/-7.6% of arterioles in control versus 62.7+/-5.5% after smoke exposure ), Despite evidence of continued deoxyribonucleic acid synthesis in the peribr onchiolar vessels, the alterations of vascular physiology previously found in this model cannot be ascribed to increased reactivity at this site. Inst ead, the chronic deoxyribonucleic acid synthesis in the arterioles adjacent to the alveolar ducts, culminating in an increased number of fully: muscul arized vessels, would suggest this compartment as the most probable source.