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Am. J. Respir. Crit. Care Med., Volume 158, Number 6, December 1998, 1900-1906

Differences in Airway Closure between Normal and Asthmatic Subjects Measured with Single-Photon Emission Computed Tomography and Technegas

GREGORY G. KING, STEFAN EBERL, CHERYL M. SALOME, IVEN H. YOUNG, and ANN J. WOOLCOCK

Institute of Respiratory Medicine and Department of Medicine, University of Sydney; and Departments of Respiratory Medicine and PET and Nuclear Medicine, Royal Prince Alfred Hospital, Camperdown, Australia

The absence of a maximal dose-response plateau as well as gas trapping and increases in closing capacity (CC) suggest that increased airway closure is an important mechanical abnormality of asthmatic airways. We compared the extent and distribution of airway closure in 13 normal and in 23 asthmatic subjects. Airway closure (LVclosed) was measured with single-photon emission computed tomography (SPECT) and an inhaled Technegas bolus as the percentage of lung volume without Technegas (LVtrans), and with CC, using nitrogen washout. LVclosed was compared in the apical, middle and lower zones, each being of equal vertical height. Values of mean LVclosed ± 95% confidence interval (CI) were similar in normal (30 ± 6.0% LVtrans) and asthmatic subjects (30 ± 7.8% LVtrans). In normal subjects, LVclosed correlated with both age (r = 0.89, p < 0.01) and CC (r = 0.86, p < 0.01), was more extensive in the lower zone (58 ± 18.8% LVtrans, p < 0.01) than in the middle and upper zones (17 ± 8.7% and 26 ± 8.2 LVtrans, respectively), and increased with age in both the middle and lower zones (r = 0.94 and r = 0.90, respectively, p < 0.01). In asthmatic subjects, LVclosed did not correlate with age; was greatest in the lower zone, intermediate in the middle zone, and lowest in the apical zone (59 ± 13.2%, 22 ± 5.8%, and 12 ± 4.4% LVtrans, respectively, p < 0.01); and correlated weakly with age in the middle zone only (r = 0.46, p < 0.05). We conclude that there is a predictable pattern of airway closure in normal subjects and that it is primarily influenced by pulmonary elastic recoil. This pattern is lost in asthmatic subjects. This may be explained by an increased range of closing pressures and a patchy distribution of airway closure, probably secondary to allergic inflammation.




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