OBJECTIVETo observe the protective role of the ectogenesis zinc in the rat flap with ischemia-reperfusion injury and study the mechanism.

METHODSAn abdominal island flap was created in Wistar rats. 48 rats were randomly divided into three groups, 16 per group: the non-ischemia-reperfusion group, the ischemia-reperfusion group and the ischemia-reperfusion (IR) group treated with zinc. The content of malondialdehyde (MDA) and the activity of myeloperoxidase (MPO) were measured. The expression of metallothionein (MT) was observed, and the image analysis was performed. The ultrastructure changes of the skin flap with ischemia-reperfusion injury and the flap viability were observed.

RESULTSCompared with the IR group, at 1 h and 24 h of reperfusion, the level of MDA in the adding-zinc-IR group decreased 11.3% and 33.2% (P < 0.05); the activity of MPO decreased 14.2% and 22.7% (P < 0.05); the content of MT increased 41.5% and 44% ( P < 0.01) respectively. In the ischemia-reperfusion injury flaps, MT was located in the cytoplasm of many kinds of cells. The ultrastructure changes of the skin flap of the adding-zinc-IR group were slighter than those of the IR group. The flap viability in the adding-zinc-IR group increased 27.2% (P < 0.05).

CONCLUSIONSMT could be induced by ectogenesis zinc in the flap of rats. The flap with ischemia-reperfusion injury was protected by MT through protecting the cells in the flap.