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J Appl Physiol 103: 1463, 2007; doi:10.1152/japplphysiol.00703.2007
8750-7587/07 $8.00
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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 view of the Viewpoint by Solbert Permutt (3) in this issue of the Journal of Applied Physiology, it is becoming clear that the extent of decline in pulmonary function in asthmatics is not a simple function of the degree of smooth muscle shortening, but is the manifestation of complicated relationships among baseline airway structure, the degree of airway smooth muscle shortening, and compensatory changes in lung volumes. In this case, increases in total lung capacity and functional residual capacity minimized the impact of the observed increase in residual volume on the decline in pulmonary function (1).

We showed that in a mouse model of asthma, acute increases in airway wall thickness due to airway inflammatory effects leading to airway closure (and presumably change in lung volume) is the cause of airways hyperresponsiveness (AHR), not increased contractility of airway smooth muscle (2, 5). The study by Brown et al. (1) shows that airway structure and lung volumes are important determinants of AHR and pulmonary function in humans as well. Furthermore, Venegas et al. (4) showed that asthmatics have disturbed ventilation distribution that can be understood in terms of airway closure. These findings suggest a link between airway structure and its function that manifests as a change in lung volumes, irrespective of the model system used. Hence, we concur with Dr. Permutt that lung volumes are highly related to airway function in asthmatics and we believe an important determinant of AHR in both mice and humans.

FOOTNOTES


Address for reprint requests and other correspondence: H. C. Haverkamp, Univ. of Vermont, College of Medicine, 149 Beaumont Ave., HSRF 226, Burlington, VT 05405 (e-mail: hans.haverkamp{at}uvm.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. Lundblad LK, Thompson-Figueroa J, Allen GB, Rinaldi L, Norton RJ, Irvin CG, Bates JH. Airways hyperresponsiveness in allergically inflamed mice: the role of airway closure. Am J Resp Crit Care Med 175: 768–774, 2007.[Abstract/Free Full Text]
  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. 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]
  5. Wagers S, Haverkamp HC, HC, Bates JHT, Norton RJ, Thompson-Figueroa JA, Sullivan MJ, Irvin CG. Intrinsic and antigen-induced airway hyperresponsiveness are the result of diverse physiological mechanisms. J Appl Physiol 102: 221–230, 2007.[Abstract/Free Full Text]

Hans Christian Haverkamp
Lennart Karl Alf Lundblad
University of Vermont, College of Medicine, Burlington, Vermont





This Article
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Right arrow Articles by Lundblad, L. K. A.


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