Inflammatory reaction in pulmonary muscular arteries of patients with mildchronic obstructive pulmonary disease

Endothelial dysfunction and intimal thickening have been shown in pulmonary arteries (PA) of patients with mild chronic obstructive pulmonary disease (COPD). To investigate whether an inflammatory process related to tobacco s moking might be involved in the development of pulmonary vascular abnormali ties in COPD, we characterized the inflammatory cell infiltrate and the end othelium-dependent relaxation in PA of 39 patients who underwent lung resec tion, divided into three groups: "nonsmokers" (n = 7); "smokers," with norm al lung function (n = 12); and "COPD" (n = 20). Endothelium-dependent relax ation was assessed in vitro by exposing PA rings to adenosine diphosphate ( ADP). Inflammatory cell types were identified by immunohistochemistry. PA o f COPD patients developed lower relaxation in response to ADP than nonsmoke rs and smokers. The number of inflammatory cells was increased in PA of COP D compared with the other two groups. This cell infiltrate was largely cons tituted by T lymphocytes. The CD8(+) T-cell subset was increased in both sm okers and COPD compared with nonsmokers, yielding a reduction of the CD4(+) /CD8(+) ratio. The intensity of the inflammatory infiltrate correlated with both the endothelium-dependent relaxation and the intimal thickness. We co nclude that cigarette smoking induces a CD8(+) T-lymphocyte infiltrate in P A, which is associated with the impairment of the vessel's structure and fu nction, suggesting the potential involvement of an inflammatory process in the pathogenesis of pulmonary vascular abnormalities in the early stage of COPD.