The physiological consequences of altered airways structure on the function of asthmatic airways has been of interest to clinicians and physiologists since the classic study of Huber and Koessler in 1922.1 These authors provided the first measurements of airway wall thickness in relation to their size and reported that the airway wall of patients who died of asthma was thicker than that of controls. Many have subsequently commented on this finding,2-7 and Freedman provided an excellent review of its functional significance in 1972.8 A systematic analysis of the effect of wall thickening on airway function by Moreno and colleagues showed that a thickening of the inner aspect of the airway wall that had little or no effect on baseline airways resistance was capable of amplifying the effect of smooth muscle shortening on airway calibre to account for the airways hyperresponsiveness of asthmatic subjects.9 A series of studies followed that further explored this problem using both quantitative histology and computer based models of the airways.10-15 Wiggset al 15 used a computer model to argue that the greatest effect of the combination of smooth muscle shortening and wall thickening on the reduction of airway calibre is in the peripheral airways because these structures are encircled by airway smooth muscle. Yanai et al 16subsequently investigated the site of increased resistance in human airways using direct measurements of pressure and flow to establish that the peripheral airways were the major site of lower airway obstruction in asthma.

In this issue of Thorax Orsida and colleagues17 provide information on the nature of the vascular changes in bronchial biopsy specimens, arguing that the observations made in the bronchi reflect those in the smaller airways. They compare biopsy tissue from a control group with that from two groups of asthmatic patients—one treated and the other not treated with inhaled steroids—and show an increase in the number of vessels and total area of submucosa occupied by vessels in the biopsy specimens from patients with asthma. They also found that inhaled steroids reduced the area of the submucosa occupied by vessels in the asthmatic patients without influencing the number of vessels observed.

This study extends the available data on airway vasculature in asthma18-21 and is consistent with the concept that the inflammatory response that underlies asthma increases the submucosal vascular compartment, possibly by inducing the growth of new vessels. The authors argue that these vascular changes alter airways function because they found that the change in number of vessels/mm²of lamina propria induced by steroids correlated with the percentage change in forced expiratory volume in one second (FEV₁) after bronchodilator and the airways response to inhaled methacholine. They suggest that a positive effect of inhaled steroids may be in reducing the size of this vascular compartment, but recognise that this finding will need to be confirmed by future longitudinal and interventional studies before being fully accepted. However, the possibility that the inflammatory process responsible for asthma results in vascular congestion with proliferation of new vessels and that these changes influence airway function is an interesting one that deserves to be fully investigated.