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1 Depts of Pharmacology and Clinical Pharmacology, and 2 Anatomy with Radiology, University of Auckland, and 3 Dept of Histopathology, Auckland Hospital, Auckland, New Zealand.
CORRESPONDENCE: P. N. Black, Dept of Pharmacology and Clinical Pharmacology, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. Fax: 64 93737556. E-mail: pn.black{at}auckland.ac.nz
Keywords: Chronic obstructive pulmonary disease, elastin, emphysema, histology, small airways
Received: February 12, 2007
Accepted January 15, 2008
Small airways are the major site of airflow obstruction in chronic obstructive pulmonary disease (COPD). This is attributed to loss of elastin in alveoli and fibrosis in small airways. In the present study, it was hypothesised that changes to elastic fibres in alveoli might be paralleled by a similar reduction in elastic fibres in small airways.
Tissue blocks from patients who had lobectomy for bronchial carcinoma were studied. Patients were classified as COPD (forced expiratory volume in one second (FEV1) <80% predicted, FEV1/forced vital capacity (FVC) <0.7) or controls (FEV1
The v/f for elastic fibres in alveoli was 18.6% for COPD and 32.8% in controls. In the airways the v/f was 14.6% for COPD and 25.5% in controls. FEV1% predicted was correlated with v/f in both alveoli and small airways.
The volume fraction of elastic fibres was reduced to a similar extent in small airways and alveoli in chronic obstructive pulmonary disease and both were correlated with the extent of airflow obstruction. Loss of elastic fibres in small airways may contribute to the development of airflow obstruction in chronic obstructive pulmonary disease.
80% pred, FEV1/FVC
0.7). Elastic fibres were visualised using Elastic van Gieson staining and the volume fraction (v/f) of elastic fibres was determined as a percentage of tissue volume using point counting. Elastic fibre networks were also visualised by confocal microscopy.
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