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Regarding Anesthetics, Lung Function, and Models of Obesity

Tharp, William G. MD, PhD

doi: 10.1213/ANE.0000000000001345
Letters to the Editor: Letter to the Editor

Published ahead of print June 9, 2016

Department of Anesthesiology, University of Vermont Medical Center University of Vermont College of Medicine, Burlington, Vermont, william.tharp@uvmhealth.org

Published ahead of print June 9, 2016

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To the Editor:

Heil et al1 have performed a study that elegantly links altered body composition and anesthetic drug selection to detrimental changes in lung function. However, their choice of the term “diet-induced obesity” could be misleading to the clinician because there was no difference in body weight between the rodents in the “obese” and lean groups, only a difference in body adiposity and composition. They have chosen a diet-resistant model, that is, one with no weight gain despite hypercaloric feeding, more relevant to the metabolic syndrome than to chronic obesity. There are multiple standard diets and protocols for inducing weight-gain and obesity in rodents, as well as validated genetic models of rodent obesity that the authors could have chosen to ensure obesity was the primary focus.2 Also, the propofol lipid emulsion carrier cannot be ruled out as an important causative agent of lung inflammation.3,4 Was consideration given to using water-soluble fospropofol or coinfusion of the carrier emulsion with dexmedetomidine or thiopental as a control?

This study is an interesting and important addition to our understanding of metabolic dysfunction and potential complications of anesthesia, but it needs to be made clear that these results are not generalizable to obese humans. Future studies need to incorporate standard models of obesity and control for the potential effects of the propofol lipid emulsion before attempting to examine the mechanisms involved.

William G. Tharp, MD, PhD

Department of Anesthesiology

University of Vermont Medical Center

University of Vermont College of Medicine

Burlington, Vermont

william.tharp@uvmhealth.org

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REFERENCES

1. Heil LB, Santos CL, Santos RS, Samary CS, Cavalcanti VC, Araujo MM, Poggio H, de A Maia L, Trevenzoli IH, Pelosi P, Fernandes FC, Villela NR, Silva PL, Rocco PR. The effects of short-term propofol and dexmedetomidine on lung mechanics, histology, and biological markers in experimental obesity. Anesth Analg 2016;122:1015–23.
2. Tschöp M, Heiman ML. Rodent obesity models: an overview. Exp Clin Endocrinol Diabetes 2001;109:307–19.
3. Driscoll DF, Ling PR, Andersson C, Bistrian BR. Hepatic indicators of oxidative stress and tissue damage accompanied by systemic inflammation in rats following a 24-hour infusion of an unstable lipid emulsion admixture. JPEN J Parenter Enteral Nutr 2009;33:327–35.
4. Hecker M, Linder T, Ott J, Walmrath HD, Lohmeyer J, Vadász I, Marsh LM, Herold S, Reichert M, Buchbinder A, Morty RE, Bausch B, Fischer T, Schulz R, Grimminger F, Witzenrath M, Barnes M, Seeger W, Mayer K. Immunomodulation by lipid emulsions in pulmonary inflammation: a randomized controlled trial. Crit Care 2015;19:226.
© 2016 International Anesthesia Research Society