Share this article on:

In Response

Heil, Luciana Boavista MD; Pelosi, Paolo MD; Silva, Pedro L. PhD; Rocco, Patricia R. M. MD, PhD

doi: 10.1213/ANE.0000000000001343
Letters to the Editor: Letter to the Editor

Published ahead of print June 9, 2016

Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil, Department of Surgical and Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil

IRCCS AOU San Martino-IST, Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy

Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil, prmrocco@gmail.com

Published ahead of print June 9, 2016

We sincerely thank Dr. Tharp for his interest in our study1 and important comments concerning the obesity model and propofol carrier emulsion. His first concern is that we used a model of altered adiposity and not diet-induced obesity. We offered animals a carbohydrate-enriched diet (based on palatable confectionary product made from sweetened milk) to better mimic the Western human diet (the cafeteria diet) for 120 days. Because rats have a higher basal metabolic rate than humans, this time course corresponds to approximately 11 years in humans.2 Even though body weight did not differ significantly between control and obese animals, we believe that this did not represent a diet-resistant model. All animals exhibited changes in body composition and metabolic, hormonal, and proinflammatory profiles (triglyceride, total cholesterol, insulin, and leptin levels) not usually observed in diet-resistant animals.3 Because there is no validated body mass index analog or waist/hip ratio for use in rats, evaluating animal models based on the same criteria used in humans is of questionable validity.4 A classification of obesity in small animals has yet to be defined, but parameters seen in the human obese population, that is, metabolic, hormonal, and proinflammatory changes, have to be considered.5

The second concern is that the propofol carrier might have affected our results. We cannot rule out that the propofol carrier emulsion may indeed induce changes in lung mechanics and inflammation. A widely available commercial propofol formulation was used in our study. It is important to dissociate the harmful effect observed with this formulation from those of propofol (2,6-diisopropylphenol) proper. We agree that testing the prodrug fospropofol in future experiments will be valuable. However, this study represented a first step toward better understanding the role of propofol in experimental obesity and obtaining new insights about its possible effects in obese patients. Further experimental studies are required to assess the potential impact of fospropofol on lung function and inflammation, as well as to clarify the interactions between propofol and hyperleptinemia or adipocytokines in obesity.

Luciana Boavista Heil, MD

Laboratory of Pulmonary Investigation

Carlos Chagas Filho Biophysics Institute

Federal University of Rio de Janeiro

Rio de Janeiro, Rio de Janeiro, Brazil

Department of Surgical and Sciences

Federal University of Rio de Janeiro

Rio de Janeiro, Brazil

Paolo Pelosi, MD

IRCCS AOU San Martino-IST

Department of Surgical Sciences and Integrated Diagnostics

University of Genoa

Genoa, Italy

Pedro L. Silva, PhD

Patricia R. M. Rocco, MD, PhD

Laboratory of Pulmonary Investigation

Carlos Chagas Filho Biophysics Institute

Federal University of Rio de Janeiro

Rio de Janeiro, Brazil

prmrocco@gmail.com

Back to Top | Article Outline

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. West D, West BJ. Physiologic time: a hypothesis. Phys Life Rev 2013;10:210–24.
3. Levin BE, Triscari J, Hogan S, Sullivan AC. Resistance to diet-induced obesity: food intake, pancreatic sympathetic tone, and insulin. Am J Physiol 1987;252:R471–8.
4. Kennedy AJ, Ellacott KL, King VL, Hasty AH. Mouse models of the metabolic syndrome. Dis Model Mech 2010;3:156–66.
5. Thibault L, Woods SC, Westerterp-Plantenga MS. The utility of animal models of human energy homeostasis. Br J Nutr 2004;92(suppl 1):S41–5.
© 2016 International Anesthesia Research Society