岛状皮瓣缺血再灌注损伤的血液流变学改变及地塞米松的调理研究

HEMORHEOLOGY OF ISLAND FLAP AFTER ISCHEMIA-REPERFUSION INJURY AND MODULATION OF DEXAMETHASONE

目的 探讨岛状皮瓣缺血再灌注损伤中血液流变学的变化及地塞米松的调理作用机制。方法 采用Wister大鼠 6 0只 ,等分为缺血再灌注损伤模型。对照组 ( 组 )腹腔注射生理盐水 2 ml/ kg,实验组 ( 组 )腹腔注射地塞米松 5 mg/ kg。术后 7天观察皮瓣成活面积 ;电镜观察皮瓣超微结构 ,计数中性粒细胞的坏死数量 ;以血液流变检测仪检测红细胞流变学 ,以微循环检测仪及扫描电镜检测中性粒细胞的流变学。结果 皮瓣成活面积 组显著大于 组 ;术后1、2天时 ,中性粒细胞的坏死数量 组显著少于 组 (P<0 .0 5 ) ;全血低切黏度、红细胞聚集指数、Casson屈服应力及中性粒细胞的黏附性 组明显高于 组 (P<0 .0 5 ) ;中性粒细胞的变形性 组则比 组低。结论 皮瓣缺血再灌注损伤可引起红细胞聚集性增强 ,中性粒细胞黏附性增加、变形性能力下降和坏死数量增多 ;地塞米松可有效调理上述指标 ,减少中性粒细胞的坏死数量 。

Objective To study the hemorheology of island flap after ischemia reperfusion injury and modulation of dexamethasone. Methods Sixty Wister rats were made ischemia reperfusion injury model, and divided into two groups randomly(Group I: intraperitoneal injection of normal saline 2 ml/kg as control group; Group II: intraperitoneal injection of dexamethasone 5 mg/kg as experimental group). Flap survived areas were measured and neutrophil necrosis numbers in flaps were counted. Erythrocytes and neutrophil hemorheology were observed. Results Area survived flap in group II was larger than that in group I. Neutrophil necrosis numbers were less in group II than in group I ( P< 0 05). Whole blood hyposhear viscosity, erythrocyte aggregation, Casson yield stress and nerutrophil adhesion ability were higher in group I than in group II ( P< 0 05); and the neutrophil deformability was lower in group I than in group II. Conclusion Flap inchemia reperfusion can increase erythrocyte aggregation index and neutrophil adhesion ability. Dexamethasone can improve these and decrease neutrophil necrosis numbers, so as to prevent flap from ischemia reperfusion injury.