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J Appl Physiol 103: 1464, 2007; doi:10.1152/japplphysiol.00702.2007
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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: In his Viewpoint, Dr. Permutt (5) offers the intriguing hypothesis that in asthma, narrowing of large airways causes dynamic hyperinflation with an increase in total lung capacity (TLC), which in turn limits a further adaptive increase in TLC during air trapping associated with activation of airway smooth muscle. It seems unlikely, however, that the magnitude of the reductions in large airway diameter reported by Dr. Permutt and colleagues (1) would increase the expiratory time constant sufficiently to cause dynamic hyperinflation during normal tidal breathing. Alternatively, the link between large airway diameter and hyperinflation may be indirect. Airway obstruction and air trapping in asthma is heterogeneous, as visualized by hyperpolarized gas magnetic resonance imaging (2, 3), with ventilation defects smaller than would be expected were the predominant obstruction in the large airways. However, model simulations predict that constriction in the central airways may result in destabilization of clusters of peripheral airways, with resulting patches of ventilation defects occurring at the level of terminal bronchioles (6). In addition to air trapping distal to closed and severely constricted airways, hyperinflation could result from tonic activation of inspiratory muscles, which occurs as a reflex or adaptive response to bronchoconstriction (4). Thus hyperinflation associated with reduced large airway diameter would not necessarily implicate the large airways as the primary site of obstruction. Whether a preexisting increase in TLC renders a person more vulnerable to acute bronchoconstriction remains an interesting question to be investigated.

FOOTNOTES


Address for reprint requests and other correspondence: R. Sorkness, 777 Highland Ave., Madison, WI 53705 (e-mail: rlsorkne{at}wisc.edu)

REFERENCES

  1. Brown RH, Pearse DB, Pyrgos G, Liu MC, Togias A, Permutt S. The structural basis of airways hyperresponsiveness in asthma. J Appl Physiol 101: 30–39, 2006.[Abstract/Free Full Text]
  2. de Lange EE, Altes TA, Patrie JT, Gaare JD, Knake JJ, Mugler JP III, Platts-Mills TA. Evaluation of asthma with hyperpolarized helium-3 MRI: correlation with clinical severity and spirometry. Chest 130: 1055–1062, 2006.[CrossRef][Web of Science][Medline]
  3. Fain SB, Korosec FR, Holmes JH, O'Halloran R, Sorkness RL, Grist TM. Functional lung imaging using hyperpolarized gas MRI. J Magn Reson Imaging 25: 910–923, 2007.[CrossRef][Web of Science][Medline]
  4. Martin J, Powell E, Shore S, Emrich J, Engel LA. The role of respiratory muscles in the hyperinflation of bronchial asthma. Am Rev Respir Dis 121: 441–447, 1980.[Web of Science][Medline]
  5. Permutt S. The role of the large airways on smooth muscle contraction in asthma. J Appl Physiol; doi:10.1152/japplphysiol.00568.2007.
  6. Venegas JG, Winkler T, Musch G, Vidal Melo MF, Layfield D, Tgavalekos N, Fischman AJ, Callahan RJ, Bellani G, Harris RS. Self-organized patchiness in asthma as a prelude to catastrophic shifts. Nature 434: 777–782, 2005.[CrossRef][Medline]

Ronald Sorkness
 Department of Pharmacy Medicine and Pediatrics, University of Wisconsin, Madison, Wisconsin





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