Quantitative and morphological analysis of the vascular bed in bronchial biopsy specimens from asthmatic and non-asthmatic subjects.

BACKGROUND This study was designed to establish the number and area (as a percentage) of bronchial wall vessels in subjects with and without asthma, to obtain information on the morphology of the vessels, and to see whether changes differed in patients with mild, moderate, and severe asthma. METHODS Biopsy specimens were taken using a rigid bronchoscope from the carina of the middle lobe bronchus of 20 patients with allergic asthma and 20 non-asthmatic controls. Specimens were sectioned and stained with haematoxylin-eosin, Masson trichrome, PAS, alcian blue-PAS, and orcein. The vessels were counted and the vascular area was calculated as a percentage in the lamina propria, in blind conditions, on PAS stained sections in 50 microscopic fields (magnification x1000, 0.02 mm(2) per field). The vascular area was calculated using the points counting procedure (Chalkley point array). The vascular morphology, intravascular cells, and the perivascular area were also studied using a magnification up to x1200. RESULTS Patients with asthma had more vessels (mean (SD) 226.70 (74.53) v 172.05 (30.58), p=0.0043) and a larger percentage vascular area (8.61 (2.38)% v 6.81 (2.25)%, p=0.028) than non-asthmatic subjects. Patients with severe asthma had significantly more vessels than those with mild or moderate disease (p=0.0044). Asthmatic capillaries and venules had oedematous walls and thickening of the subendothelial basement membrane, and hypotrophic or atrophic myocytes and fibrosis in the arterioles. Vessels from asthmatic subjects showed eosinophil recruitment, activation, and intravascular lysis. Intense eosinophil recruitment was associated with more marked vascular structural changes. Muscular formations protruded into the lumen in the arterioles of both groups, and in asthmatics these had hypotrophic or atrophic myocytes and fibrosis. CONCLUSIONS Morphometric analysis showed that the bronchial lamina propria of asthmatic subjects had a larger number of vessels, occupying a larger percentage area than in non-asthmatic subjects. The number of vessels was correlated with the severity of the asthma. Marked alterations to the vascular structure appeared to be associated with intense eosinophil recruitment and intravascular activation. This is the first report of asthmatic and non-asthmatic bronchial wall specimens containing intra-arteriolar muscular formations, presumably to regulate blood flow to the capillary network and/or sinusoids. This function might be impaired when these structures are remodelled in asthmatic patients.