The effect of stromal vascular fraction in an experimental frostbite injury model.

Background: Despite current treatment modalities, frostbite remains an injury with a poor prognosis which may cause functional morbidities. Several experimental and clinical studies have demonstrated that stromal vascular fraction is an autologous mixture, which can improve wound healing and vasculogenesis. The aim of this study was to show the beneficial effects of stromal vascular fraction on experimental frostbite healing.

Material And Methods: Stromal vascular fraction (SVF) was harvested from 5 rats after excision of the inguinal fat pads. Another 20 rats were separated into 2 groups of 10 as the SVF group and the control group. A frostbite injury was created on each rat using a cryoprobe frozen with liquid nitrogen (-196 °C). SVF was applied to the SVF group and phosphate-buffered saline to the control group. All injections were performed subcutaneously within the frostbite injury area. Biopsies were performed on days 5 and 14 for histopathological and immunochemical evaluations. The tissue perfusion rates of both groups were assessed on day 14 using indocyanine green angiography (SPY system).

Results: The increase in mean tissue perfusion was 373.3% ( ± 32.1) in the SVF group and 123.8% ( ± 16.3) in the control group (p < 0.001). The macroscopic wound reduction rates of the SVF and control groups were 25.5% ( ± 19.1) and 18.0% ( ± 5.9), respectively on day 5%, and 78.2% ( ± 9.2) and 57.3% ( ± 16.7) on day 14 (p = 0.007; p = 0.003). Acute inflammation and the fibrosis gradient were significantly decreased in the SVF group compared to the control group (p = 0.004, p = 0.054 respectively on day 14). Granulation tissue amount, re-epithelialization score and neovascularization were significantly increased in the SVF group (p = 0.006, p = 0.010 and p = 0.021, respectively on day 14).

Conclusions: The study results demonstrated that SVF increases frostbite wound healing by increasing tissue perfusion rate, neovascularization and re-epithelialization, and modulating acute inflammation and fibrosis.