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Hyperbaric oxygen treatment prevents up‐regulation of angiogenesis following partial‐thickness skin grafts in the pig
Author(s) -
Kalns John E.,
Dick Edward J.,
Scruggs Julie P.,
Kieswetter Kris,
Wright Jim K.
Publication year - 2003
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.2003.11210.x
Subject(s) - neovascularization , angiogenesis , epidermis (zoology) , skin grafting , cell growth , vascular endothelial growth factor , wound healing , growth factor , medicine , chemistry , surgery , andrology , vegf receptors , anatomy , receptor , biochemistry
We hypothesized that hyperbaric oxygen treatment (HBO) would reduce neovascularization following partial‐thickness skin grafting in the Yucatan pig. Results show that capillary density 4 days postgraft is increased twofold in grafts not treated with HBO, compared to normal, ungrafted skin or skin grafts from pigs treated with HBO, p < 0.05. Similarly, the expression of vascular endothelial growth factor, a growth factor associated with neovascularization, was also reduced by HBO. Cell density in the graft boundary increased gradually after grafting, reaching a maximum 2.7‐fold increase, relative to normal skin, at day 4, p < 0.05. Cell nuclei positive for proliferating cell nuclear antigen, a marker of proliferation, increased threefold by day 2, p < 0.05, and then declined to normal levels by day 7. HBO had no effect on cell density or proliferation in the boundary region or on shear strength of the graft. In the epidermis, proliferation declined 80% 2 days after grafting and then returned to levels observed in normal skin by day 4, p < 0.05; however, in pigs treated with HBO, we observed no decline in proliferation. These findings confirm the hypothesis that HBO reduces neovascularization in the partial‐thickness skin graft while preserving regenerative capacity in the graft boundary and normal proliferative capacity of the epidermis. (WOUND REP REG 2003;11:139–144)