Airway secretion and asthma.

Accessible online at: http://BioMedNet.com/karger Asthma is a disease of unknown cause that tends to affect predominantly the airways. Components of the asthmatic syndrome include acute and chronic bronchospasm and evidence of airway inflammation. Patients who die of asthma are often noted to have signs of severe airway abnormalities including plugging with mucus and thickening of the airway wall. The airway is a dynamic organ and, besides conducting the flow of air, it contains a complex secretory apparatus and is obviously involved in lung defense. Because of the derangements seen in asthma, it is logical to suspect that measurement of airway clearance would be affected in the asthmatic syndrome. Using various techniques, investigators have measured clearance of secretions from the asthmatic lung and, consistent with the unknown nature of asthma, observations of airway clearance in this disease have been variable. Indeed, within a given group of asthmatic subjects, mucociliary clearance measurements have been defined as ‘normal’, ‘abnormal or reduced’ and finally ‘increased’ or faster than normal. It is likely that some of these differences are related to the technical aspects of clearance measurement. While rigorous criteria for assessing the initial sites of deposition of radiolabeled particles and the techniques for analyzing retention curves have not been set, some observations probably reflect the disease process. We know that hospitalized asthmatic patients have markedly impaired clearance of retained aerosols from the lung [1]. With treatment, clearance can return towards normal but in chronic asthma many patients appear to have impaired clearance primarily from central airways [2]. A subset of asthmatics do appear to have mucociliary clearance that is more rapid than normal [3]. In the present issue of Respiration, Svartengren et al. [4] have measured mucociliary clearance using radiolabeled aerosols and a recently modified technique of ‘very slow inhalation’. Under these circumstances particles are thought not to deposit in the ‘central airways’ because of reduced forces of inertial impaction. They settle predominantly in airways thought by these authors to be distal bronchioles. In their asthmatic patients, these particles appear to be retained for a longer period of time than in normal subjects indicating that the ‘small airways’ of these patients were abnormal both in the resting state and after an induced bronchoconstriction. The technique utilized by Svartengren et al. [4] has several advantages in that the collimated detectors are very sensitive and the amount of radioactivity necessary to label airway mucus is very low. The sensitivity of these detectors also enables prolonged observation over a longer period of time than that generally utilized by the Á camera. However, the technique does lack regional sensitivity. For example, we do not really know where these airways are. Future studies combining their technique with Á camera imaging may be helpful. While the clearance of radiolabeled aerosols from Svartengren’s patients was not different after allergen bronchoprovocation, it is possible that the sites of deposition were different. Following allergen inhalation even with reversal of the FEV1, particles may have deposited more centrally. Local inflammatory effects might have impaired clearance, but a direct comparison with control airways was not possible. In spite of these limitations, the study does demonstrate that relatively asymptomatic asthmatic patients have abnormal clearance.