Kanika Jetmalani1,2, David G Chapman3,4,5, Cindy Thamrin3,4, Claude S Farah3,4,6, Norbert Berend3,4,7, Cheryl M Salome3,4, Gregory G King3,4,8. 1. Woolcock Institute of Medical Research, Glebe, New South Wales, Australia. Kanika.jetmalani@sydney.edu.au. 2. Sydney Medical School, The University of Sydney. Kanika.jetmalani@sydney.edu.au. 3. Woolcock Institute of Medical Research, Glebe, New South Wales, Australia. 4. Sydney Medical School, The University of Sydney. 5. Vermont Lung Centre, University of Vermont College of Medicine, Burlington, Vermont, United States. 6. Department of Respiratory Medicine, Concord Hospital, Concord. 7. Department of Respiratory Research, George Institute of Global Health. 8. Department of Respiratory Medicine, Royal North Shore Hospital, Sydney, New South Wales, Australia.
Abstract
BACKGROUND AND OBJECTIVE: Cigarette smoke exposure increases airway smooth muscle (ASM) contractility. Abnormalities in peripheral airway function in smokers with normal spirometry could be due to the effects of ASM tone. We aimed to determine the contribution of ASM tone to peripheral airway function in smokers with normal spirometry from the response to bronchodilator (BD). METHODS: Ventilation heterogeneity in peripheral conductive (Scond) and acinar (Sacin) airways were measured in 50 asymptomatic smokers and 20 never-smokers using multiple breath nitrogen washout, before and 20 min after inhalation of 200 µg salbutamol and 80 µg ipratropium bromide. Z-scores were calculated to define abnormality in Sacin and Scond. RESULTS: Nineteen smokers had abnormal Sacin, and 12 had abnormal Scond; 7 had abnormalities in both. After BD, Sacin improved in smokers with normal Sacin (6.5 ± 15.9%, P = 0.02), smokers with abnormal Sacin (9.2 ± 16.9%, P = 0.03) and in control subjects (11.7 ± 18.2%, P = 0.01), with no differences in improvements between groups. Sacin remained abnormal in 15/19 smokers and their post-BD values correlated with smoking exposure (r = 0.53, P = 0.02). After BD, Scond improved in smokers with abnormal Scond (28.3 ± 15.9%, P = 0.002) and normalized in 9/12 subjects, but not in those with normal Scond (0.25 ± 32.7%, P = 0.44) or control subjects (-1.7 ± 21.2%, P = 0.64). CONCLUSION: In smokers with normal spirometry, abnormal conductive airway function could be attributed to increased bronchomotor tone. In contrast, bronchomotor tone in acinar airways is unaffected by smoking and functional abnormality. There may be different causal mechanisms underlying acinar and conductive airway abnormalities in smokers with normal spirometry.
BACKGROUND AND OBJECTIVE: Cigarette smoke exposure increases airway smooth muscle (ASM) contractility. Abnormalities in peripheral airway function in smokers with normal spirometry could be due to the effects of ASM tone. We aimed to determine the contribution of ASM tone to peripheral airway function in smokers with normal spirometry from the response to bronchodilator (BD). METHODS: Ventilation heterogeneity in peripheral conductive (Scond) and acinar (Sacin) airways were measured in 50 asymptomatic smokers and 20 never-smokers using multiple breath nitrogen washout, before and 20 min after inhalation of 200 µg salbutamol and 80 µg ipratropium bromide. Z-scores were calculated to define abnormality in Sacin and Scond. RESULTS: Nineteen smokers had abnormal Sacin, and 12 had abnormal Scond; 7 had abnormalities in both. After BD, Sacin improved in smokers with normal Sacin (6.5 ± 15.9%, P = 0.02), smokers with abnormal Sacin (9.2 ± 16.9%, P = 0.03) and in control subjects (11.7 ± 18.2%, P = 0.01), with no differences in improvements between groups. Sacin remained abnormal in 15/19 smokers and their post-BD values correlated with smoking exposure (r = 0.53, P = 0.02). After BD, Scond improved in smokers with abnormal Scond (28.3 ± 15.9%, P = 0.002) and normalized in 9/12 subjects, but not in those with normal Scond (0.25 ± 32.7%, P = 0.44) or control subjects (-1.7 ± 21.2%, P = 0.64). CONCLUSION: In smokers with normal spirometry, abnormal conductive airway function could be attributed to increased bronchomotor tone. In contrast, bronchomotor tone in acinar airways is unaffected by smoking and functional abnormality. There may be different causal mechanisms underlying acinar and conductive airway abnormalities in smokers with normal spirometry.
Authors: Jack Bozier; Edward Jeagal; Paul D Robinson; G Kim Prisk; David G Chapman; Gregory G King; Cindy Thamrin; Sandra Rutting Journal: ERJ Open Res Date: 2022-07-18
Authors: Hooria Alowiwi; Stella Watson; Kanika Jetmalani; Cindy Thamrin; David P Johns; E Haydn Walters; Gregory G King Journal: BMC Pulm Med Date: 2022-05-28 Impact factor: 3.320
Authors: Kanika Jetmalani; Nathan J Brown; Chantale Boustany; Brett G Toelle; Guy B Marks; Michael J Abramson; David P Johns; Alan L James; Michael Hunter; Arthur W Musk; Norbert Berend; Claude S Farah; David G Chapman; Cindy Thamrin; Gregory G King Journal: ERJ Open Res Date: 2021-11-08