Assessment of Airway Tone in Asthma: Comparison Between Double Lung Transplant Patients and Healthy Subjects

N. A. Molfino; A. S. Slutsky; G. Julià-Serdà; V. Hoffstein; J. P. Szalai; K. R. Chapman; A. S. Rebuck; N. Zamel

doi:10.1164/ajrccm/148.5.1238

journal article Nov 01, 1993

Assessment of Airway Tone in Asthma: Comparison Between Double Lung Transplant Patients and Healthy Subjects

N. A. Molfino A. S. Slutsky G. Julià-Serdà V. Hoffstein J. P. Szalai K. R. Chapman A. S. Rebuck N. Zamel

American Review of Respiratory Disease Vol. 148 No. 5 pp. 1238-1243 · Oxford University Press (OUP)

View at Publisher Save 10.1164/ajrccm/148.5.1238

Abstract

Abstract
We investigated the hypothesis that asthmatic patients have an increased cholinergic tone by measuring tracheobronchial cross-sectional areas during transient voluntary apnea. This allowed us to assess bronchomotor tone without the influence of changes in lung recoil or lung volume. Three groups of subjects with potentially different levels of tracheobronchial tone were studied: 14 healthy volunteers (N), 18 stable asthmatic patients (A), and 10 double lung transplant recipients (T). Using the acoustic reflection technique, we measured changes in tracheobronchial cross-sectional areas during short periods (5 to 10 s) of voluntary apnea. In a subset of subjects, studies were repeated before and after the inhalation of the muscarinic antagonist ipratropium. During breath-holding, glottis and extrathoracic trachea remained unchanged but intrathoracic trachéal area decreased by 30 ± 8% (mean ± standard error of the mean) in N, by 27 ± 3% in A, and by 9 ± 4% in the T group. Bronchial areas decreased by 24 ± 8% in N, by 45 ± 3% in A, and by 10 ± 4% in T. These differences among groups were statistically significant at the trachéal and bronchial levels (p &lt; 0.05), and ipratropium significantly inhibited this airway constriction (p &lt; 0.05) only in the asthmatic group. Assuming that changes in cross-sectional airway areas during voluntary apnea reflect airway tone, these results support the view that in humans this tone is mainly vagally controlled and that it is significantly increased in asthmatic compared with nonasthmatic subjects.

Topics

No keywords indexed for this article. Browse by subject →

References

58

[1]

Roy CS J Physiol (Lond) (1885)

[2]

Barnes PJ Am Rev Respir Dis (1986)

[3]

Woolcock AJ. Philadelphia: W. B. Saunders (1988)

[4]

Bronchial reactivity to inhaled histamine: a method and clinical survey

D. W. Cockcroft, D. N. KILLIAN, J. J. A. MELLON et al.

Clinical & Experimental Allergy 10.1111/j.1365-2222.1977.tb01448.x

[5]

10.1056/nejm199012203232505

[6]

10.1146/annurev.ph.45.030183.002321

[7]

10.1016/0091-6749(82)90038-0

[8]

10.1378/chest.89.3.414

[9]

10.1056/nejm198608213150803

[10]

Fish JE J Appl Physiol (1983) 10.1152/jappl.1983.54.1.105

[11]

10.1007/bf02718145

[12]

10.1159/000194388

[13]

Boulet L-P Am Rev Respir Dis (1984)

[14]

10.1016/0091-6749(84)90488-3

[15]

10.1164/ajrccm/138.4.765

[16]

10.1136/thx.44.3.161

[17]

Green M J Appl Physiol (1974) 10.1152/jappl.1974.37.6.793

[18]

Fish JE J Appl Physiol (1981) 10.1152/jappl.1981.50.5.1079

[19]

Hahn HL J Appl Physiol (1976) 10.1152/jappl.1976.41.4.581

[20]

Widdicombe JG J Appl Physiol (1963) 10.1152/jappl.1963.18.4.681

[21]

Mitchell GS J Appl Physiol (1985) 10.1152/jappl.1985.59.1.198

[22]

D'Urzo AD Am Rev Respir Dis (1987)

[23]

D'Urzo AD J Appl Physiol (1988) 10.1152/jappl.1988.64.1.367

[24]

10.1164/ajrccm/136.1.225

[25]

Patterson GA Clinics in Chest Medicine. Philadelphia: W. B. Saunders (1990) 10.1016/s0272-5231(21)00690-0

[26]

Hoftstein V Eur Respir J (1991)

[27]

Zamel N Bull Eur Physiopathol Respir (1984)

[28]

Dolovich MB Ltd. (1985)

[29]

Hoftstein V Am Rev Respir Dis (1984)

[30]

D'Urzo AD J Appl Physiol (1986) 10.1152/jappl.1986.60.2.398

[31]

Rubinstein I J Appl Physiol (1987) 10.1152/jappl.1987.63.4.1469

[32]

Jackson AC J Appl Physiol (1977) 10.1152/jappl.1977.43.3.523

[33]

Jackson AC J Appl Physiol (1980) 10.1152/jappl.1980.48.5.896

[34]

Jackson AC J Appl Physiol (1981) 10.1152/jappl.1981.50.6.1286

[35]

Jackson AC J Appl Physiol (1984) 10.1152/jappl.1984.57.2.351

[36]

Rubinstein I Am Rev Respir Dis (1988) 10.1164/ajrccm/138.5.1164

[37]

Molfino NA Am Rev Respir Dis (1991)

[38]

Katz I J Appl Physiol (1988) 10.1152/jappl.1988.65.6.2390

[39]

Molfino NA Am Rev Respir Dis (1992) 10.1164/ajrccm/146.3.577

[40]

Nadel JA New York: Dekker (1980)

[41]

Vidruk EH J Appl Physiol (1985) 10.1152/jappl.1985.59.3.941

[42]

Loofbourrow GN Am J Physiol (1957) 10.1152/ajplegacy.1957.191.2.411

[43]

Edmunds LH J Appl Physiol (1971) 10.1152/jappl.1971.31.5.722

[44]

10.1164/ajrccm/140.1.58

[45]

Springall DR Am Rev Respir Dis (1990) 10.1164/ajrccm/141.6.1538

[46]

Stretton CD Am Rev Respir Dis (1990) 10.1164/ajrccm/142.5.1030

[47]

Widdicombe JG Am Rev Respir Dis (1991) 10.1164/ajrccm/143.3_pt_2.s18

[48]

Boskabady MH Am Rev Respir Dis (1992) 10.1164/ajrccm/145.4_pt_1.756

[49]

Cuss FMC New York: Dekker (1990)

[50]

Douglas JS Am Rev Respir Dis (1990) 10.1164/ajrccm/141.3_pt_2.s123

Showing 50 of 58 references

Metrics

67

Citations

58

References

Details

Published: Nov 01, 1993
Vol/Issue: 148(5)
Pages: 1238-1243
License: View

Authors

N

N. A. Molfino