Significance of reactive oxygen species in distal flap necrosis and its salvage with liposomal SOD.

In an attempt to elucidate whether reactive oxygen species (ROS) have a role in causing distal necrosis of random pattern flaps, and to develop measures to prevent necrosis, three experiments were made using a rat flap model. The flap-salvaging effect of liposomal superoxide dismutase (L-SOD) was assessed. The results were as follows: (1) Measurements of changes in cutaneous blood flow in a flap, with time, revealed an initial remarkable decrease followed by gradual but significant increase in the distal portion 24 hours after operation. (2) The SOD activity in the flap continued to decrease gradually with time until 24 hours after operation both in L-SOD treated and control groups. However, SOD activity in L-SOD treated flaps was always significantly higher than in the control. (3) S-D value (survival length minus dye distance) was significantly greater in the L-SOD treated flap than in the control flap, indicating a significant effect of L-SOD in preventing the expected flap necrosis. These results suggest a possible role, in causing flap necrosis, of ROS which are generated by reperfusion following ischaemia, and the effectiveness of L-SOD in salvaging distal flap necrosis.