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American Journal of Respiratory and Critical Care Medicine Vol 175. pp. 95, (2007)
© 2007 American Thoracic Society


Correspondence

Interpreting Lung Functional Changes

To the Editor:

The recent article by Tsuchida and colleagues (1) addresses an important issue in lung pathophysiology. The attempt to link molecular signaling to the functional and structural changes after lung injury is highly commendable. However, there is an issue with the analysis of lung mechanics presented that warrants further consideration.

The pressure–volume (PV) curves published in Figure 9 of this article are quite unusual. In fact, they have an appearance that has not been previously seen. The fact that the curves show the inflation and deflation limbs fully superimposed at high pressure must reflect some sort of experimental or analytic artifact. Lungs are never at a maximal volume at 25 cm H2O, and the almost sudden flattening of the inflation limb and superimposition with the deflation limb is not what happens in rodent or other mammalian lungs (24). It is also surprising that the complete loops from the edematous injured lungs show complete closure on deflation.

In addition to these concerns about the abnormal appearance of curves themselves, the conclusions drawn from the curves are also questionable. To say that the static compliance of the lungs is decreased simply because one hasn't inflated the lungs as much doesn't really tell us very much about the lung. If one looks at the "lavaged injurious" inflation limb, at 25 cm H2O, the curve still hasn't begun to flatten (assuming the sudden sharp turn at 25 is indeed an artifact). Finally, even if all these concerns were resolved, the PV curves would still be difficult to interpret, since they were started from a variable volume (i.e., the end-expiratory volume). Their highly nonlinear nature by itself would make the slope less at higher volume, in addition to reducing the inspiratory capacity (which the authors interpreted as a change in lung properties). Increased fluid mass in the lung does not necessarily imply atelectasis. Although the air volume at end expiration was measured in other animals, part of the alveolar volume in the injured lung will be fluid, and it is the total alveolar volume that will determine the PV characteristics. In general, if one wants to use PV curves to interpret lung properties, the absolute alveolar volume needs to be anchored to some known value.

Wayne Mitzner

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland

FOOTNOTES

Conflict of Interest Statement: W.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

REFERENCES

  1. Tsuchida S, Engelberts D, Peltekova V, Hopkins N, Frndova H, Babyn P, McKerlie C, Post M, McLoughlin P, Kavanagh BP. Atelectasis causes alveolar injury in nonatelectatic lung regions. Am J Respir Crit Care Med 2006;174:279–289.[Abstract/Free Full Text]
  2. Tankersley CG, Rabold R, Mitzner W. Differential lung mechanics are genetically determined in inbred murine strains. J Appl Physiol 1999;86:1764–1769.[Abstract/Free Full Text]
  3. Jones TA, Petsonk EL, Frazer DG. Effect of temperature on pressure-volume hysteresis of excised lungs. Respir Physiol 1996;106:47–55.[CrossRef][Medline]
  4. Faridy EE, Permutt S. Surface forces and airway obstruction. J Appl Physiol 1971;30:319–321.[Medline]




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2007 American Thoracic Society