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Mechanisms of Action of External Volume Expansion Devices

Lancerotto, Luca M.D.; Chin, Michael S. M.D.; Freniere, Brian M.D.; Lujan-Hernandez, Jorge R. M.D.; Li, Qiong M.D., Ph.D.; Vasquez, Alessandro Valderrama M.Sc.; Bassetto, Franco M.D.; Del Vecchio, Daniel A. M.D.; Lalikos, Janice F. M.D.; Orgill, Dennis P. M.D., Ph.D.

Plastic and Reconstructive Surgery: September 2013 - Volume 132 - Issue 3 - p 569–578
doi: 10.1097/PRS.0b013e31829ace30
Experimental: Original Articles
Video Discussion

Background: External volume expansion by suction has been proposed to improve the survival of fat grafting by preparing the recipient site. In previous experimental work, external volume expansion demonstrated the capacity to stimulate cell proliferation, vessel remodeling, and adipogenesis. This study investigated possible mechanisms underlying these observed changes.

Methods: A miniaturized external volume expansion device was applied to the dorsum of mice for 2 hours. Hypoxia during stimulation was assessed with pimonidazole hydrochloride, and tissue perfusion was measured for up to 2 days using hyperspectral imaging. Treated tissues were evaluated by microscopy for edema, inflammation, and the effects on cell proliferation and vessel remodeling.

Results: External volume expansion–treated tissues were grossly expanded with 2 hours of stimulation, developing a macroscopic swelling that regressed slowly over the course of hours following stimulus cessation. This gross swelling was reflective of histologic signs of intense edema, persistent for at least 1 hour after external volume expansion. Tissues were hypoxic during stimulation, and hyperspectral imaging demonstrated decreased tissue content of both oxygenated and deoxygenated hemoglobin in the first hour after external volume expansion release. The onset of inflammation was already apparent by the end of stimulation and remained elevated through 2 days after external volume expansion. At this time point, epidermal and dermal cell proliferation and vascular density were significantly increased.

Conclusion: External volume expansion sets in motion various mechanisms, including mechanical stimulation, edema, ischemia, and inflammation, that over distinct time periods maintain an environment conducive to cell proliferation and angiogenesis, which can be elicited even by a single 2-hour external volume expansion cycle.

VIDEO DISCUSSION BY GEOFFREY C. GURTNER, M.D., IS AVAILABLE ONLINE FOR THIS ARTICLE.

Boston and Worcester, Mass.; and Padova, Italy

From the Tissue Engineering and Wound Healing Laboratory, Division of Plastic Surgery, Brigham and Women’s Hospital and Harvard Medical School; the Institute of Plastic, Reconstructive and Aesthetic Surgery, University of Padova; the Division of Plastic Surgery, University of Massachusetts Medical School; and Back Bay Plastic Surgery.

Received for publication October 16, 2012; accepted February 4, 2013.

Presented in part at the Fourth European Plastic Surgery Research Council, in Hamburg, Germany, August 23 through 26, 2012; the 10th Anniversary Meeting of the International Federation for Adipose Therapeutics and Science, in Quebec City, Quebec, Canada, October 5 through 7, 2012; and the Fourth International Conference on Regenerative Surgery, in Rome, Italy, December 13 through 15, 2012.

Disclosure:Dr. Orgill has been an expert witness, consultant, and grant recipient of funding provided by Kinetic Concepts, Inc., the manufacturer of the devices used in this study. The other authors have no financial interest to declare in relation to the content of this article.

A Video Discussion by Geoffrey C. Gurtner, M.D., accompanies this article. Go to PRSJournal.com and click on “Video Discussions” in the “Videos” tab to watch.

Dennis P. Orgill, M.D., Ph.D., Division of Plastic Surgery, Brigham and Women’s Hospital, 75 Francis Street, Boston, Mass. 02115, dorgill@partners.org

©2013American Society of Plastic Surgeons