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.

Mechanisms of action of External Volume Expansion devices.

LANCEROTTO, LUCA;BASSETTO, FRANCO;
2013

Abstract

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.
File in questo prodotto:
File Dimensione Formato  
00006534-201309000-00012.pdf

accesso aperto

Tipologia: Published (publisher's version)
Licenza: Accesso libero
Dimensione 1.02 MB
Formato Adobe PDF
1.02 MB Adobe PDF Visualizza/Apri
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2659306
Citazioni
  • ???jsp.display-item.citation.pmc??? 19
  • Scopus 75
  • ???jsp.display-item.citation.isi??? 73
  • OpenAlex ND
social impact