Department of Respiratory Medicine, Royal North Shore Hospital, St. Leonards, NSW, Australia.
Airway Physiology and Imaging Group, The Woolcock Institute of Medical Research, The University of Sydney, NSW, Australia.
J Appl Physiol (1985). 2020 Jan 1;128(1):168-177. doi: 10.1152/japplphysiol.00482.2019. Epub 2019 Nov 21.
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 ( = 9) and subjects without obesity ( = 10) underwent baseline and postbronchoprovocation SPECT-CT imaging, in which Technegas was inhaled upright and followed by supine scanning. Lung regions that were nonventilated (Vent), low ventilated (Vent), or well ventilated (Vent) 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, Vent and Vent for the entire lung were similar in subjects with and without obesity. However, in the upper lung zone, Vent (17.5 ± 10.6% vs. 34.7 ± 7.8%, < 0.001) and Vent (25.7 ± 6.3% vs. 33.6 ± 5.1%, < 0.05) were decreased in subjects with obesity, with a consequent increase in Vent (56.8 ± 9.2% vs. 31.7 ± 10.1%, < 0.001). The greater diversion of ventilation to the upper zone was correlated with body mass index ( = 0.74, < 0.001), respiratory system resistance ( = 0.72, < 0.001), and respiratory system reactance ( = -0.64, = 0.003) but not with lung volumes or basal airway closure. Following bronchoprovocation, overall Vent increased similarly in both groups; however, in subjects without obesity, Vent only increased in the lower zone, whereas in subjects with obesity, Vent 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. 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.
肥胖与肺容积减少有关,这可能导致在潮气呼吸时气道关闭增加和通气分布异常。我们使用单光子发射计算机断层扫描(SPECT)-计算机断层扫描(CT)研究了肥胖对健康受试者在乙酰甲胆碱诱导的支气管收缩前后通气的拓扑分布的影响。肥胖受试者(n=9)和非肥胖受试者(n=10)接受基线和支气管激发后 SPECT-CT 成像,吸入 Technegas 后取直立位和仰卧位扫描。使用自适应阈值方法计算未通气(Vent)、低通气(Vent)或通气良好(Vent)的肺区,并以占总肺容积的百分比表示。为了确定区域通气,将肺分为轴向长度的上、中、下三分之一,从 CT 获得。在基线时,肥胖和非肥胖受试者的整个肺的 Vent 和 Vent 相似。然而,在上肺区,肥胖受试者的 Vent(17.5±10.6%比 34.7±7.8%, < 0.001)和 Vent(25.7±6.3%比 33.6±5.1%, < 0.05)降低,导致 Vent 增加(56.8±9.2%比 31.7±10.1%, < 0.001)。通气向肺上区的更大转移与体重指数( =0.74, < 0.001)、呼吸系统阻力( =0.72, < 0.001)和呼吸系统电抗( =-0.64, = 0.003)相关,但与肺容积或基础气道关闭无关。支气管激发后,两组的总体 Vent 均增加,但非肥胖受试者仅在下肺区增加 Vent,而肥胖受试者的 Vent 则均匀增加。总之,肥胖与基线和支气管激发后通气分布的改变有关,这与肺容积减少无关。我们使用健康受试者的通气 SPECT-CT 成像,证明肥胖时的通气被转移到上肺区,这与体重指数密切相关,但与功能残气容积和气道关闭无关。此外,在非肥胖者中,仅在下肺区发生乙酰甲胆碱诱导的支气管收缩,而在肥胖者中,它均匀分布在所有肺区。这些发现表明肥胖相关因素改变了通气的拓扑分布。