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Depts of 1 Pulmonary Medicine and 2 Pathology, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Hospital Clínic, University of Barcelona
CORRESPONDENCE: J.A. Barberà, Servei de Pneumologia, Hospital Clínic, Villarroel, 170 08036, Barcelona, Spain. Fax: 34 932275455. E-mail: jbarbera@clinic.ub.es
Keywords: chronic obstructive pulmonary disease, pulmonary artery, pulmonary hypertension, tobacco smoke
Received: May 21, 2001
Accepted October 31, 2001
This study was supported by grants from the Fondo de Investigación Sanitaria (FIS 99/188 and 00/922), Sociedad Española de Neumología y Cirugía Torácica (SEPAR-1999) and Generalitat de Catalunya (1999SGR-228). S. Santos is the recipient of research fellowship awards from the Hospital Clínic of Barcelona and SEPAR. V.I. Peinado is supported by the Comissió Interdepartamental de Recerca i Innovació Tecnològica and the Fundació Clínic per a la Recerca Biomèdica.
Intimal enlargement of pulmonary arteries is an early change in chronic obstructive pulmonary disease (COPD). The cellular and extracellular components that are involved in this enlargement are unknown. The present study was designed to characterize the structural changes occurring in pulmonary muscular arteries in the initial disease stages.
Lung specimens from patients with moderate COPD (n=8; forced expiratory volume in one second (FEV1), 66±10% predicted) and smokers without airflow obstruction (n=7; FEV1, 86±6% pred), were investigated by histochemistry to characterize extracellular matrix proteins and by immunohistochemistry to identify intrinsic cells of the vascular wall.
In both COPD patients and smokers, the majority of cells present in the enlarged intimas were stained by specific smooth muscle cell (SMC) markers. No staining with endothelial or fibroblast markers was shown. A proportion of SMCs did not stain with desmin, suggesting cellular heterogeneity in this population. Elastin was the most abundant extracellular matrix protein and collagen was seen in a lower proportion. The amount of collagen was related to the intimal thickness (p<0.001).
The findings demonstrated smooth muscle cell proliferation, as well as elastin and collagen deposition, in the thickened intimas of pulmonary arteries in moderate chronic obstructive pulmonary disease patients and smokers, suggesting that these abnormalities may originate at an early stage in cigarette smoke-induced respiratory disease.
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