Obesity alters the topographical distribution of ventilation and the regional response to bronchoconstriction

Author:

Rutting S.12,Mahadev S.12,Tonga K. O.1234,Bailey D. L.45,Dame Carroll J. R.2,Farrow C. E.246,Thamrin C.2,Chapman D. G.27,King G. G.128

Affiliation:

1. Department of Respiratory Medicine, Royal North Shore Hospital, St. Leonards, NSW, Australia

2. Airway Physiology and Imaging Group, The Woolcock Institute of Medical Research, The University of Sydney, NSW, Australia

3. Department of Thoracic and Transplant Medicine, St. Vincent's Hospital, Darlinghurst, NSW, Australia

4. Faculty of Medicine & Health, University of Sydney, NSW, Australia

5. Department of Nuclear Medicine, Royal North Shore Hospital, St. Leonards, NSW, Australia

6. Department of Respiratory Medicine, Westmead Hospital, Westmead, NSW, Australia

7. School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW, Australia

8. NHMRC Centre of Excellence in Severe Asthma, New Lambton Heights, NSW, Australia

Abstract

Obesity is associated with reduced operating lung volumes that may contribute to increased airway closure during tidal breathing and abnormalities in ventilation distribution. We investigated the effect of obesity on the topographical distribution of ventilation before and after methacholine-induced bronchoconstriction using single-photon emission computed tomography (SPECT)-computed tomography (CT) in healthy subjects. Subjects with obesity ( n = 9) and subjects without obesity ( n = 10) underwent baseline and postbronchoprovocation SPECT-CT imaging, in which Technegas was inhaled upright and followed by supine scanning. Lung regions that were nonventilated (Ventnon), low ventilated (Ventlow), or well ventilated (Ventwell) were calculated using an adaptive threshold method and were expressed as a percentage of total lung volume. To determine regional ventilation, lungs were divided into upper, middle, and lower thirds of axial length, derived from CT. At baseline, Ventnon and Ventlow for the entire lung were similar in subjects with and without obesity. However, in the upper lung zone, Ventnon (17.5 ± 10.6% vs. 34.7 ± 7.8%, P < 0.001) and Ventlow (25.7 ± 6.3% vs. 33.6 ± 5.1%, P < 0.05) were decreased in subjects with obesity, with a consequent increase in Ventwell (56.8 ± 9.2% vs. 31.7 ± 10.1%, P < 0.001). The greater diversion of ventilation to the upper zone was correlated with body mass index ( rs = 0.74, P < 0.001), respiratory system resistance ( rs = 0.72, P < 0.001), and respiratory system reactance ( rs = −0.64, P = 0.003) but not with lung volumes or basal airway closure. Following bronchoprovocation, overall Ventnon increased similarly in both groups; however, in subjects without obesity, Ventnon only increased in the lower zone, whereas in subjects with obesity, Ventnon increased more evenly across all lung zones. In conclusion, obesity is associated with altered ventilation distribution during baseline and following bronchoprovocation, independent of reduced lung volumes. NEW & NOTEWORTHY Using ventilation SPECT-computed tomography imaging in healthy subjects, we demonstrate that ventilation in obesity is diverted to the upper lung zone and that this is strongly correlated with body mass index but is independent of operating lung volumes and of airway closure. Furthermore, methacholine-induced bronchoconstriction only occurred in the lower lung zone in individuals who were not obese, whereas in subjects who were obese, it occurred more evenly across all lung zones. These findings show that obesity-associated factors alter the topographical distribution of ventilation.

Funder

Lung Foundation Australia

Northern sydney local health district

Department of Health, Australian Government | National Health and Medical Research Council

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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