This study aims to explore the probable mechanism of better result of dural reconstruction by CO2 laser soldering and the effect of exogenous basic fibroblast growth factor (bFGF) or transforming growth factor-beta1(TGF beta(1)) on wound healing. In part I of the study, ten minipigs were randomized into two equal groups, and the dural defects were reconstructed by conventional fibrin glue (FG) bonding (group I (a)) or by CO2 laser soldering (group I-b). In part II, 36 minipigs were randomized into three equal groups, and the dural defect was reconstructed by CO2 laser soldering; then exogenous bFGF or TGF beta(1) was administered in group IIb and group IIc, respectively, while group IIa served as control group. The dural specimens were harvested at 1st week postoperatively in part I; and at 1st, 2nd, 3rd, and 4th week postoperatively in part II, they were examined for healing condition and subjected to hematoxylin-eosin (HE) staining and immunohistochemical (IHC) staining with antibodies against bFGF and TGF beta(1). In part I, group I-b showed higher fibroblast cell density than group I-a (P < 0.05). The optical density (OD) for IHC staining with antibodies against bFGF of group I-b was significantly higher than that of group I-a (P < 0.05), and for IHC staining with antibodies against TGF beta(1), group I-b showed positive staining while group I-a was negative. In part II, administering exogenous bFGF or TGF beta(1) made a left shift of fibroblast cell number-time curve compared with control group. For specimens' IHC staining with antibodies against bFGF, the OD of group IIb was higher than that of group IIa in the corresponding time. For specimens' IHC staining with antibodies against TGF beta(1), the OD of groups IIb and IIc was both higher than that of group IIa (P < 0.05 and P < 0.01, respectively). In conclusion, CO2 laser may trigger fibroblast proliferation through stimulating the secretion of bFGF and TGF beta(1). Topically administering exogenous bFGF or TGF beta(1) could accelerate the healing of the reconstructed dura by enhancing secretion of bFGF and/or TGF beta(1) and promoting the process of fibroblast gathering-degrading.