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J Appl Physiol 103: 1460, 2007; doi:10.1152/japplphysiol.00684.2007
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LETTER TO THE EDITOR

Commentary on "The role of the large airways on smooth muscle contraction in asthma"

TO THE EDITOR: Dr. Permutt (3) hypothesizes that the response to constrictor agents in asthma is the result of large-to-medium airways narrowing, leading to a decrease of vital capacity (VC) and, in turn, of 1-s forced expiratory volume (FEV1). The fall in VC could be due to an increase in residual volume (RV), unless total lung capacity (TLC) also increases, thus compensating for the fall in lung function. The hypothesis opens questions that need to be addressed. If it is known that TLC increases with exacerbations (5), its changes with acute administration of bronchoconstrictor or bronchodilator agents are generally regarded as technical artifacts. Perusal of Dr. Brown and colleagues' data (1) reveals that the decrease in TLC after albuterol could be due either to a too high frequency of panting during measurement of thoracic gas volume or, alternatively, to a decrease in lung elastic recoil (Pel). Unfortunately, neither reason for the TLC increase can be ruled out. Against theoretical predictions on flow dynamics, changes in FEV1 failed to correlate with changes in bronchial diameter. Yet this may not be surprising in view of the dependency of FEV1 on thoracic gas compression, Pel, effects of deep breath, and TLC, all of these being affected by disease and medications. Finally, Dr. Permutt's hypothesis on the site of bronchoconstriction in asthma has to be reconciled with the many imaging, functional, and modeling studies suggesting that it is heterogeneous constriction of the distal airways that is central to the disease (2, 4).

FOOTNOTES


Address for reprint requests and other correspondence: V. Brusasco, Dept. of Internal Medicine, Univ. of Genoa, Respiratory Pathophysiology Unit, Padiglione Maragliano, Ospedale San Martino, Largo R. Benzi, 10, 16132 Genova, Italy (e-mail: vito.brusasco{at}unige.it)

REFERENCES

  1. Brown RH, Pearse DB, Pyrgos G, Liu MC, Togias Alkis, Permutt S. The structural basis of airways hyperresponsiveness in asthma. J Appl Physiol 101: 30–39, 2006.[Abstract/Free Full Text]
  2. Downie SR, Salome CM, Verbanck S, Thompson BR, Berend N, King GG. Ventilation heterogeneity is a major determinant of airway hyperresponsiveness in asthma, independent of airway inflammation. Thorax 2007 [Epub ahead of print].
  3. Permutt S. The role of the large airways on smooth muscle contraction in asthma. J Appl Physiol; doi:10.1152/japplphysiol.00568.2007.
  4. Tgavalekos NT, Tawhai M, Harris RS, Musch G, Vidal-Melo M, Venegas JG, Lutchen KR. Identifying airways responsible for heterogeneous ventilation and mechanical dysfunction in asthma: an image functional modeling approach. J Appl Physiol 99: 2388–2397, 2005.[Abstract/Free Full Text]
  5. Woolcock AJ, Read J. Lung volumes in exacerbations of asthma. Am J Med 41: 259–273, 1966.[CrossRef][Web of Science][Medline]

Riccardo Pellegrino1
Vito Brusasco2
 1Centro di Fisiopatologia Respiratoria e dello Studio della Dispnea, Azienda Ospedaliera S. Croce e Carle, Cuneo; and 2Dipartimento di Medicina Interna, Università di Genova, Genova, Italy





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