Rebuttal from Dr. Bates

Abstract

POINT-COUNTERPOINTRebuttal from Dr. BatesPublished Online:01 Nov 2007https://doi.org/10.1152/japplphysiol.00369.2007bMoreSectionsPDF (37 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Dr. Mitzner and I clearly differ in our opinions about the usefulness of lung impedance (4, 6). However, we do agree on certain key things, such as the lack of utility of Penh, which, as my worthy opponent rightly points out, has seduced many investigators solely on account its ease of use (1). But then he makes the error of suggesting that this unfortunate state of affairs also applies to impedance because equipment is now available to measure it with relative ease (6). While there is no question that a certain amount of confusion currently reigns over the physiological interpretation of lung impedance, this is not a reflection of any fundamental shortcoming in the quantity itself. Rather, the shortcoming resides in the community of scientists who use it. Indeed, Dr. Mitzner says as much, for example, when he accuses investigators of lack of consistency in the use of the constant-phase model parameter G (6). As I stated previously (4), in a homogeneous lung G reflects the dissipative properties of the lung tissues. However, both analytical investigation (2) and simulation studies with anatomically accurate models of the lung (5, 7) have shown that changes in G relative to H (tissue elastance) can be used to infer the development of lung derecruitment versus regional ventilation heterogeneities. These are nontrivial physiological insights that, along with those provided by RN (airway resistance) and H, have been used to advantage in several recent studies (e.g., Refs. 3, 5, 8). Dr. Mitzner also charges that “investigators often just extract airway resistance from the impedance” (6). This is true, but again it simply reflects ignorance, not fundamental futility. If investigators choose to discard some of the information present in an experimental measurement, the fault (if there is any) lies with them. To be fair, lung impedance can only be properly interpreted in physiological terms in the context of a mathematical model of the lung (5, 7). This introduces a level of technical complexity that goes beyond what many biomedical researchers are used to, which probably explains how far we have not come in 30 years (6). The utility of impedance thus comes down to an issue of intellectual accessibility, which is consequently its greatest impediment to widespread acceptance. Nevertheless, I firmly believe that an appreciation of the utility of lung impedance is potentially within the grasp of any trained scientist and well worth the effort.REFERENCES1 Bates J, Irvin C, Brusasco V, Drazen J, Fredberg J, Loring S, Eidelman D, Ludwig M, Macklem P, Martin J, Milic-Emili J, Hantos Z, Hyatt R, Lai-Fook S, Leff A, Solway J, Lutchen K, Suki B, Mitzner W, Pare P, Pride N, Sly P. The use and misuse of Penh in animal models of lung disease. Am J Respir Cell Mol Biol 31: 373–374, 2004.Crossref | PubMed | ISI | Google Scholar2 Bates JH, Allen GB. The estimation of lung mechanics parameters in the presence of pathology: a theoretical analysis. Ann Biomed Eng 34: 384–392, 2006.Crossref | PubMed | ISI | Google Scholar3 Bates JH, Wagers SS, Norton RJ, Rinaldi LM, Irvin CG. Exaggerated airway narrowing in mice treated with intratracheal cationic protein. J Appl Physiol 100: 500–506, 2006.Link | ISI | Google Scholar4 Bates JHT. Point: Lung impedance measurements are more useful than simpler measurements of lung function in animals models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007.Google Scholar5 Lutchen KR, Greenstein JL, Suki B. How inhomogeneities and airway walls affect frequency dependence and separation of airway and tissue properties. J Appl Physiol 80: 1696–1707, 1996.Link | ISI | Google Scholar6 Mitzner W. Counterpoint: Lung impedance measurements are not more useful than simpler measurements of lung function in animals models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007a.Google Scholar7 Thorpe CW, Bates JH. Effect of stochastic heterogeneity on lung impedance during acute bronchoconstriction: a model analysis. J Appl Physiol 82: 1616–1625, 1997.Link | ISI | Google Scholar8 Wagers S, Lundblad LK, Ekman M, Irvin CG, Bates JH. The allergic mouse model of asthma: normal smooth muscle in an abnormal lung? J Appl Physiol 96: 2019–2027, 2004.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 103Issue 5November 2007Pages 1903-1904 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00369.2007bHistory Published online 1 November 2007 Published in print 1 November 2007 Metrics