Involvement of reactive oxygen species in post-ischaemic flap necrosis and its prevention by antioxidants.

In attempts to substantiate the possible participation of reactive oxygen species, and the significance of the xanthine oxidase system in both post-ischaemic reperfusion necrosis of the island flap and distal necrosis of the pedicle flap, and to develop new pharmacological measures for salvaging flap necrosis, a series of experiments were made using an island flap model and a random-pattern flap model in rats. The results were as follows: (1) Epoxysuccinyl derivative (E-64c), allopurinol and L-SOD salvaged post-ischaemic reperfusion necrosis of the island flaps; (2) E-64c and allopurinol did not salvage anticipated necrosis of the distal region of random flaps but L-SOD did; (3) tissue SOD activity did not reflect the fate of the island flap, but did of the distal region of the random flap. These results demonstrated a possible involvement of ROS in both post-ischaemic necrosis of island flaps and distal necrosis of random flaps. However, xanthine oxidase was significant in producing ROS only in the former.