中性粒细胞活化在缺血-再灌注损伤皮瓣微循环改变中的作用及地塞米松的调理

目的：研究皮瓣微循环超微结构的改变及活化中性粒细胞在其中的作用，阐明地塞米松保护皮瓣的作用机理。方法：Wistar大鼠分成4组，形成岛状皮瓣后，Ⅰ组：原位缝合；Ⅱ组：阻断静脉回流6h；Ⅲ组：阻断静脉回流10h；Ⅳ组：阻断静脉回流10h，去除血管夹时腹腔注射地塞米松5mg／kg。取材进行电镜和髓过氧化物酶(MPO)的检测。结果：Ⅰ组皮瓣微循环内皮细胞结构完整，无中性粒细胞粘附。术后MPO值一直为0。Ⅱ组内皮细胞肿胀，部分脱落，有一定数量活化中性粒细胞粘附于管壁。术后l、3天MPO值明显上升。Ⅲ组：内皮细胞坏死脱落。术后l天MPO值几乎是Ⅱ组的2倍。Ⅳ组内皮细胞结构基本完整，管壁少见活化中性粒细胞粘附。结论：缺血一再灌注损伤皮瓣微循环有显著的组织学改变，MPO值术后显著增加，且随阻断静脉回流时间延长而增加。中性粒细胞的活化在这一组织学改变过程中起重要作用。地塞米松保护皮瓣的机理与减轻了中性粒细胞的活化水平有关。

The role of active neutrophil on ischemia-reperfusion flap''''s microcirculatory structure and the modulation of dexamethasone

Objective To study flap's microcirculatory structure and the role of active neutrophil,elucidate protection mechanisms of dexamethsone. Methods 48 rats were divided into 4 groups equally. I: No clamps were applied on flap's pedicle vessel; II: Clamps application lasted 6 hours. Ill: Clamps were applied for 10 hours; IV: Dexamethsone were given when clamps which lasted for 10 hours had been removed. Results I: Microcirculatory' s endothelial cells were integrated.no neutrophil was adherence with endothelium, and MPO's level is 0. II: Microcirculatory showed swelled endothelial cell, some of which were lifted. Active neutrophils were adherence with endothelium. MPO's value rised obviously on the first and third day after operation. Ill: Microcirculation showed necrotic and lifted endothelial cell.MPO' s value rised nearly 2 times the first day after operation than that in II group. IV: Endothelial cells were integrated mostly, little active neutrophil showed contacted with endothelium. Conclusion Ischemia flap' s microcir-culation shows obvious histopathology. MPO rised posteperatively and correlated with venous ischemia time. Active neutrophil have important role in this process. Dexamethsone could modulate neutrophil function.