Last Word on Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease

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LETTERS TO THE EDITORLast Word on Point:Counterpoint: Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary diseaseWayne MitznerWayne MitznerPublished Online:01 Nov 2007https://doi.org/10.1152/japplphysiol.00748.2007MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat THE ABILITY TO MAKE A MEASUREMENT IS NOT A SUFFICIENT CONDITIONto the editor: After reading all the comments (2) on our debate (1, 3), it may seem that Jason has won this round, with five letters clearly in support of his position, one relatively neutral, one with lukewarm support of both of us (thank you, Ken), and one that dumped on both of us. However, of these writers, since five have had part of their careers invested in such impedance modeling, perhaps this first round vote tally is not entirely unbiased. Nevertheless, despite these otherwise thoughtful comments, still no one has told me what any measurement of G has done to improve our understanding of lung structure or pathology. This is after 15 years of making such measurements. And although Dr. Hantos tried to link G to older measures of tissue resistance, no one can even explain what the structural origins of “tissue” resistance are. Furthermore, despite Fredberg's mathematical rearrangement to focus on eta, reports of eta with experimental manipulations, mice are often as variable as they are constant. So perhaps the constant phase model as applied to the intact lung is not so constant after all.The critically important issue is that the great majority of researchers using animal models of lung disease are now making measurements of impedance for no other reason than it is now very easy (and acceptable) to do. Dr. Zeldin and colleagues suggest that we measure and report both impedance variables along with traditional R and E, but then why not also include the slope of phase III or N2 washout, or closing volume, or frequency dependence of compliance, or DLCO, or etc., etc., etc.? All of these many pulmonary function indexes might also provide improved ability to separate pathology from normal, but they are not included because they are just not so easy to measure in mice. In the recent past, many investigators with little knowledge of pulmonary function, but with a critical need to measure it, were unfortunately hoodwinked into buying snake oil (i.e., Penh). When that elusive and mysterious variable was unmasked, another system took its place that can provide indexes more acceptable to pulmonary physiologists and bioengineers. So now we have mouse asthma models reporting G and eta, without any discussion of what they mean. The primary goal of an animal model of any disease is to help learn something relevant about the disease. As I emphasized previously (1), experimental data without some meaningful link to structure and function provide little insight into what we really want to know. If investigators can't intelligently discuss what each of their measured variables means, it still seems entirely inappropriate to include them in publications or grant applications.REFERENCES1 Bates JH. Point: Lung impedance measurements are more useful than simpler measurements of lung function in animal models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007.Google Scholar2 Cohen JC, Hudak J, Fredberg JJ, Hantos Z, Zeldin DC, Card JW, Carey MA, Voltz JW, Suki B, Lutchen KR, Kaczka DW, Simon BA, Lundblad LKA. Comments on Point:Counterpoint “Lung impedance measurements are/are not more useful than simpler measurements of lung function in animal models of pulmonary disease.” J Appl Physiol; doi:10.1152/japplphysiol.00759.2007.Google Scholar3 Mitzner W. Counterpoint: Lung impedance measurements are not more useful than simpler measurements of lung function in animal models of pulmonary disease. J Appl Physiol; doi:10.1152/japplphysiol.00369.2007a.Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: W. Mitzner, 615 N. Wolfe St, Baltimore, MD 21205 (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 103Issue 5November 2007Pages 1910-1910 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00748.2007History Published online 1 November 2007 Published in print 1 November 2007 Metrics