肌皮瓣缺血再灌注期间NO、TNF-α和IL-1β含量变化及意义

目的 :探讨缺血再灌注 (I/R)期间肌皮瓣静脉血浆一氧化氮 (NO)、肿瘤坏死因子 -α(TNF -α)、白细胞介素 - 1β(IL - 1β)变化规律及其在肌皮瓣I/R损伤发生中的作用。 方法 :湖北雄性白种猪 8头 ,其中实验组及对照组各 4头。制备双侧岛状腹直肌肌皮瓣 ,实验组缺血 8h ,再灌注 4h。采用Griess重氮化反应法及放射免疫分析法检测I/R不同时点肌皮瓣静脉血浆NO、TNF -α及IL - 1β的含量。采用依赖H2 O2 反应产物比色法检测再灌注毕组织髓过氧化酶 (MPO)活性 ,并观察组织病理改变。结果 :再灌注 0 .5 ,1,2h ,实验组NO含量低于对照组 (P <0 .0 1,P <0 .0 5 ,P <0 .0 5 ) ;再灌注 1,2 ,4h ,实验组TNF -α含量高于对照组 (P均 <0 .0 1) ;再灌注 2 ,4h ,实验组IL - 1β含量高于对照组 (P均 <0 .0 1) ;再灌注毕 ,实验组MPO含量高于对照组 (P <0 .0 1)。 结论 :肌皮瓣I/R期间存在局部细胞因子网络失衡 ;内皮源性NO生成减少、促炎性细胞因子TNF -α、IL - 1β释放参与了中性粒细胞介导的I/R损伤。

Kinetics of Plasma NO,TNF-α and IL-1 Concentrations in Ischemia-reperfused Island Myocutaneous Flaps

Objective: To study the kinetics of plasma NO, TNF-α and IL-1β concentrations during ischemia-reperfusion (I/R) in island myocutaneous flaps in pigs. Methods: The epigastric myocutaneous island flaps were divided into two groups: non-ischemia-reperfusion flaps (control group, n=8); ischemia-reperfusion flaps that were subjected to 8 hours of arterial ischemia followed by 4 hours of reperfusion (I/R group, n=8). The concentration of plasma NO, IL-1β and TNF-α in venous blood of myocutaneous flap before ischemia and at 0.5, 1, 2 and 4 h after reperfusion were detected by Griess method and radioimmunoassay. Myeloperoxidase(MPO)activity and tissue histopathology were investigated four hours after reperfusion. Results: Plasma NO concentrations at 0.5, 1 and 2 h after reperfusion in I/R group were significantly decreased as compared with those in control group(P <0.01, P <0.05 and P <0.05, respectively). Plasma TNF-α concentrations at 1, 2 and 4 h after reperfusion in I/R group were significantly increased as compared with those in control group(P <0.01). Plasma IL-1β concentrations at 2 h and 4 h after reperfusion in I/R group were significantly increased as compared with those in control group(P < 0.01). After reperfusion, MPO activity in I/R group were statistically increased as compared with that in control group(P <0.01). Conclusion: NO, TNF-α and IL-1β may play important roles in the I/R injury of island myocutaneous flap. The decreasing production of endothelial NO and increasing release of TNF-α and IL-1β during the initial hours of reperfusion may account for the infiltration of neutrophil in flap.