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      Bronchodilator effect of deep inspiration and bronchoconstriction-triggered cough

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          Abstract

          Background

          Cough in the patients with cough variant asthma is triggered by bronchoconstriction, which responds to bronchodilator therapy. Following airway narrowing induced by inhaled methacholine, deep inspiration (DI) causes dilation of the airways in both asthmatic and non-asthmatic subjects. The aim of the present study was to investigate the relationship between bronchodilator effect of DI and bronchoconstriction-triggered cough.

          Methods

          We measured airway responsiveness to methacholine using partial and full flow-volume curves in 28 healthy adults. The expiratory flow at 40% above residual volume from the full forced vital capacity (MEF 40) was obtained and the volume was used as the reference volume to determine the isovolume flow from the partial curve (PEF 40). Coughs were counted for 32 min during and following the inhalation of methacholine at the provocative concentration which produced a 20% fall or more in FEV 1from the post-saline value (PC 20-FEV 1). The bronchodilator effect of DI on bronchoconstriction induced by methacholine at the PC 20-FEV 1 concentration was expressed as the ratio of (MEF 40-PEF 40)/PEF 40 (DI index).

          Results

          The number of coughs for 32 min during and following the inhalation of PC 20-FEV 1 concentration of methacholine was 39.3 ± 29.7 (mean ± SD)/32 min. The number of coughs during and following the inhalation was correlated with DI index (r = 0.57, p = 0.0015), but not with PC 20-FEV 1 or change in FEV 1 or PEF 40 by inhalation of the PC 20-FEV 1 concentration of methacholine.

          Conclusion

          We found that methacholine-induced cough was associated with the bronchodilator effect of DI on methacholine induced-bronchoconstriction in normal subjects.

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          Most cited references22

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          Increased expression of transient receptor potential vanilloid-1 in airway nerves of chronic cough.

          David A Groneberg, Akio Niimi, Q Dinh … (2004)
          Transient receptor potential vanniloid-1 (TRPV-1) mediates the cough response induced by the pepper extract capsaicin and is expressed in sensory nerves that innervate the airway wall. We determined the expression of TRPV-1 in the airways of patients with chronic persistent cough of diverse causes and with an enhanced capsaicin cough response. We obtained airway mucosal biopsies by fiberoptic bronchoscopy in 29 patients with chronic cough and 16 healthy volunteers without a cough. Immunostaining for nerve profiles with anti-protein gene product (PGP)-9.5 antibody showed no increase in nerve profiles in the airway epithelium of patients with chronic cough; however, with an anti-TRPV-1 antibody, there was a fivefold increase of TRPV-1 staining nerve profiles (p < 0.001). There was a significant correlation between capsaicin tussive response and the number of TRPV-1-positive nerves within the patients with cough. Our findings indicate that TRPV-1 receptors may contribute to an enhanced cough reflex and the cough response in chronic persistent cough of diverse causes.
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            Chronic cough as the sole presenting manifestation of bronchial asthma.

            S. Braman, W M Corrao, R. John Irwin (1979)
            Six patients with chronic cough, without history of dyspnea or wheezing, had normal base-line spirometry but hyper-reactive airways, as demonstrated with methacholine. Maintenance therapy with bronchodilators promptly eliminated the cough in all patients. Three to 12 months later therapy was discontinued for three days, cough returned, and detailed pulmonary-function studies were carried out. Again, base-line values were normal, but after methacholine one-second forced expiratory volume decreased an average of 40 per cent in the patients as compared to 30 per cent in normal controls (P less than 0.001). The point of identical flow was increased by methacholine to 43.5 per cent of vital capacity in the patients, as compared to 6 per cent in normal controls (P less than 0.001), and the alveolar plateau was 4.8 deltaN2 per liter, as compared to 1.4 in normal controls (P less than 0.01). Specific airway conductance was lowered in patients and controls, but the post-methacholine value was significantly lower in the patients. On the basis of their persistently hyper-reactive airways, inducible diffuse airway bronchoconstriction and excellent response to bronchodilator therapy, these patients appear to have a variant form of asthma in which the only presenting symptom is cough.
            Article 0 comments Cited 75 times – based on 0 reviews     Review now
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              Identification of the tracheal and laryngeal afferent neurones mediating cough in anaesthetized guinea-pigs.

              Brendan J Canning, Stuart B Mazzone, Sonya Meeker … (2004)
              We have identified the tracheal and laryngeal afferent nerves regulating cough in anaesthetized guinea-pigs. Cough was evoked by electrical or mechanical stimulation of the tracheal or laryngeal mucosa, or by citric acid applied topically to the trachea or larynx. By contrast, neither capsaicin nor bradykinin challenges to the trachea or larynx evoked cough. Bradykinin and histamine administered intravenously also failed to evoke cough. Electrophysiological studies revealed that the majority of capsaicin-sensitive afferent neurones (both Adelta- and C-fibres) innervating the rostral trachea and larynx have their cell bodies in the jugular ganglia and project to the airways via the superior laryngeal nerves. Capsaicin-insensitive afferent neurones with cell bodies in the nodose ganglia projected to the rostral trachea and larynx via the recurrent laryngeal nerves. Severing the recurrent nerves abolished coughing evoked from the trachea and larynx whereas severing the superior laryngeal nerves was without effect on coughing. The data indicate that the tracheal and laryngeal afferent neurones regulating cough are polymodal Adelta-fibres that arise from the nodose ganglia. These afferent neurones are activated by punctate mechanical stimulation and acid but are unresponsive to capsaicin, bradykinin, smooth muscle contraction, longitudinal or transverse stretching of the airways, or distension. Comparing these physiological properties with those of intrapulmonary mechanoreceptors indicates that the afferent neurones mediating cough are quite distinct from the well-defined rapidly and slowly adapting stretch receptors innervating the airways and lungs. We propose that these airway afferent neurones represent a distinct subtype and that their primary function is regulation of the cough reflex.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cough
                Title: Cough (London, England)
                Publisher: BioMed Central
                ISSN (Electronic): 1745-9974
                Publication date Collection: 2009
                Publication date (Electronic): 20 November 2009
                Volume: 5
                Page: 9
                Affiliations
                [1 ]Respiratory Medicine, Cellular Transplantation Biology, Kanazawa, University Graduate School of Medical Science, Japan
                Article
                Publisher ID: 1745-9974-5-9
                DOI: 10.1186/1745-9974-5-9
                PMC ID: 2785753
                PubMed ID: 19930579
                SO-VID: 2d53d1af-54b6-4844-a51a-15856b946ca0
                Copyright © Copyright ©2009 Ohkura et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 17 June 2009
                Date accepted : 20 November 2009
                Categories
                Subject: Research

                ScienceOpen disciplines: Respiratory medicine
                Data availability:
                ScienceOpen disciplines: Respiratory medicine

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