The authors studied the effects of basic fibroblast growth factor (b-FGF) on inflammatory angiogenesis in rats. In the corneal cauterization model b-FGF was given intra-arterially (i.a.) (carotid) and in the mesenteric window angiogenesis model, topically (i.e., intraperitoneally (i.p.)). The corneal cauterization was done under anaesthesia by topical application of silver nitrate. Mesenteric window angiogenesis was induced by injection of saline or b-FGF for four days. There were the same two groups of treatment in both models b-FGF 2.5 micrograms/kg/day or saline 1.2-5 ml/kg/day. The area of neovessels and the number of polymorphonuclear cells/field were considered for the corneal angiogenesis, the total length of neovessels was measured for the mesenteric window angiogenesis. The results were expressed as mean values (s.d.). When given i.a., b-FGF significantly reduced the number of polymorphonuclear cells three days after corneal cauterization (from 107 +/- 27 to 41.8 +/- 26, p < 0.01) and inhibited the area covered by neovessels (30 +/- 7.7% vs 51 +/- 20%, p < 0.01) after five days. In contrast, given through the extracellular space, it significantly stimulated the length of mesenteric window microvessels (169 +/- 60 mm vs 90 +/- 31 mm, p < 0.05). These results suggest that b-FGF stimulates inflammatory angiogenesis through interaction with extracellular matrix components, but inhibits it directly when given intra-arterially.