Quantitative analysis of bronchial wall vascularity in the medium and small airways of patients with asthma and COPD.
BACKGROUND
Submucosal hypervascularity is part of airway remodeling in patients with asthma; however, its existence in the small airways and its contribution to airflow limitation remain controversial.


METHODS
We investigated bronchial wall vascularity and angiogenic cells between medium airways (inner diameter, 2 to 5 mm) and small airways (inner diameter, < 2 mm) in patients with asthma (n = 9) and COPD (n = 11), and in 8 control subjects. The lung specimens obtained during surgery were immunostained to detect CD31, CD34, vascular endothelial growth factor, and basic fibroblast growth factor.


RESULTS
The number of vessels in both the medium and small airways in patients with asthma was significantly (p < 0.01) increased compared to those in patients with COPD and control subjects, and the percentage of vascularity was significantly (p < 0.01) increased in the medium airways in asthma patients and in the small airways in COPD patients. Patients with moderate asthma showed a greater increase in vascularity than those with mild asthma (p < 0.01), and the number of angiogenic factor-positive cells increased in asthma patients compared with control subjects. In asthmatic subjects, inverse correlations were found between FEV(1) percentage of predicted and the number of vessels (r = -0.85; p < 0.01), or the percentage of vascularity (r = -0.72; p < 0.03) in the inner area of the medium airways, but they were not found for the small airways. In COPD patients, no correlations were demonstrated.


CONCLUSIONS
The number of vessels in the medium and small airways in asthma patients shows a greater increase than those in COPD patients, and the vascular area in the small airways is increased in COPD patients but not in asthma patients. Enhanced vascularity in the inner area of the medium airways, but not in the small airways, might contribute to airflow limitation in asthma patients.
Hashimoto
Midori
M
Third Departments of Internal Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan.
Tanaka
Hiroshi
H
Abe
Shosaku
S
D000368:Aged; D018952:Antigens, CD34 / Q000032:analysis; D001249:Asthma / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D001980:Bronchi / Q000098:blood supply* / Q000473:pathology; D004730:Endothelium, Vascular / Q000737:chemistry; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008833:Microcirculation / Q000737:chemistry / Q000473:pathology; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
D018952:Antigens, CD34; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2