Mechanisms of dexamethasone to protect flaps from an ischemia-reperfusion injury

To study the effect of dexamethasone to protect flaps from an ischemia-reperfusion injury and elucidate its mechanism of regulating the death course of the neutrophils.

The rats were randomly divided into 3 groups. The vein of the rat was clamped for 8 h after the flap had formed. Group A: the normal flap; Group B: the saline control flap; Group C: the treatment flap with dexamethasone. The survival area of the flaps was measured at 7 days; the apoptotic and necrotic neutrophils, tumor necrosis factor alpha (TNF-alpha), and interleukin 10 (IL-10) concentrations were measured.

The flap survival areas in Groups A and C were larger than those in Group B. The apoptotic neutrophils in Group B were fewer than those in Groups A and C on the 1st and 3rd days after operation; however, they were more in number in Group B than in groups A and C on the 6th day. The necrotic cells in Group B were more in number than those in Groups A and C. In Group B, the plasma TNF-alpha concentration reached the maximum level at 1 h, while the IL-10 level reached the lowest 3 h after the reperfusion. In Group C, the TNF-alpha concentration was lower than that in Group B and decreased dramatically at 6 h. The IL10 concentration was the lowest at 1 h, and increased rapidly at 3 h. Thus, ischemia-reperfusion could injure the flaps, probably through the abnormal action of the neutrophils, such as the disordered secretion of the cytokines and abnormal death course of the neutrophils.

Dexamethasone can protect the flap from an ischemia-reperfusion injury by its regulation for the neutrophil function.