Facilitated tissue expansion with topical estriol.

Tissue expansion is a helpful technique in reconstructive plastic surgery. Unfortunately, tissue expansion still needs to be improved. Twenty-four male Wistar rats were used to evaluate the effect of estriol on tissue expansion. The agents hyaluronidase, estriol, and base cream (as a control) were applied topically to separate animal groups for 5 weeks, and their effects were studied on tissue expansion. Both hyaluronidase (p < 0.05) and estriol (p < 0.001) enhanced the rate of expansion when compared with control animals. Estriol was more effective than hyaluronidase (p < 0.05). Breaking strengths were measured in the estriol and the control groups. Breaking strength was not evaluated in the hyaluronidase group because of the necrotic changes seen at the end of the fifth week. The breaking strength was higher in the control group than in the estriol group (p < 0.05). The authors suggest that topical estriol be used as an adjunctive agent to facilitate tissue expansion.

The effect of Gingko biloba extract (Egb 761) as a free radical scavenger on the survival of skin flaps in rats. A comparative study.

Free radicals may have a role in pedicle flap necrosis. We undertook this study to compare the effect of various antioxidants and scavengers of free radicals such as vitamin E, vitamin C, deferoxamine, and Gingko biloba extract (Egb 761) on McFarlane caudal-based dorsal rat flaps. Fifty rats were divided into five groups of 10 animals each. One group served as a control (saline) group. The remaining four groups were given vitamin C 340 mg/kg, deferoxamine 150 mg/kg, Egb 761 100 mg/kg, and vitamin E 20 mg/kg. The necrosed area of flap was significantly reduced in the deferoxamine (p < 0.001), Egb 761 (p < 0.001), and vitamin C (p < 0.05) groups compared with the control group. Vitamin E had no effect on distal flap necrosis (p = 0.20).

Prevention of adriamycin-induced skin necrosis with various free radical scavengers.

Infiltration of antitumor agents into subcutaneous tissues may either result in a local area of self-resolving inflammation or progress to full-thickness loss of skin and underlying vital structures. Inadvertent extravasation of adriamycin can result in severe tissue necrosis. The mechanism of this tissue damage is believed to be release of oxygen free radicals into the tissue. After adriamycin extravasation, the treatment groups were made up according to drugs used, EGb 761, pentoxifylline, alpha-tocopherol acetate, and alpha-tocopherol succinate in rats. To prevent the necrosis and to decrease the tissue malondialdehyde levels, the most effective agent was found to be EGb 761, and pentoxifylline was also effective (P < 0.001). No difference was found between topical lanoline and saline (P > 0.05). The maximum ulcer diameter was obtained in 2 weeks. The maximum tissue malondialdehyde levels were obtained in 24 h, and in comparison to the control group the treatment groups showed lower levels. Our aim is to show the role of free radicals in the formation of skin necrosis as a cause of adriamycin extravasation and to prevent or decrease the skin necrosis using various free radical scavengers.