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Abstract
Kaposi's fibroblast growth factor (K-FGF, FGF-4) is a newer member of FGF family with uncharacterized wound healing properties. Basic fibroblast growth factor (bFGF, FGF-2) has been well studied and accelerates repair in normal and impaired wound healing models. K-FGF and bFGF are known to have similar biological effects in tissue culture, and both stimulate fibroblast and endothelial cell proliferation. The rabbit dermal ulcer model was used to examine the effects of bFGF and K-FGF under ischemic and nonischemic conditions. We found bFGF was ineffective in stimulating healing under ischemic conditions even at high doses (30 μg/wound). However, when the ischemic wounds were treated with bFGF (5 μg/wound) plus hyperbaric oxygen therapy, it was highly effective again as previously found under nonischemic conditions (P<0.05). In contrast K-FGF stimulated repair in both nonischemic and ischemic wounds (P<0.05). These results suggest that wound oxygen content differentially regulates responsiveness to bFGF and that K-FGF is biologically active in hypoxic wounds.
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