肢体缺血再灌注损伤对关节滑膜的影响

目的探讨肢体缺血再灌注(IR)对关节滑膜的损伤及其机制。方法80只新西兰大白兔随机分成正常组、缺血组和再灌注组(缺血8h后再灌注);分别于缺血后4、6、8、10h,再灌注1、3、6、12、24、72h和1、2、4、8、12周。取滑膜组织测定丙二醛(MDA)、超氧化物歧化酶(SOD)及乳酸的含量,观察形态学变化并作滑膜组织血管标记和多形核细胞(PMN)计数。结果IR早期滑膜组织有不同程度的变性和坏死,在随后的修复过程中毛细血管出现严重的狭窄和闭塞;SOD在缺血阶段即明显降低,持续到IR后8周;IR组MDA显著高于对照侧、缺血组和正常组;自缺血4h～IR2周,乳酸含量持续在高水平;PMN计数:IR组显著高于对照组。免疫组化标记显示IR8～12周血管数较健侧减少(P<0.05)。结论IR损伤早期以组织的变性坏死为主,之后患侧逐渐演变成慢性滑膜炎和创伤性关节炎。修复过程中微循环障碍及代谢产物长期滞留和PMN作用可能是影响其修复的重要因素。

Impact of ischemia-reperfusion on joint synovium in rabbits

Objective To explore the damage caused by ischemia-reperfusion (IR) to the joint synovium. Methods 80 rabbits were randomized into 3 groups. There were 5 rabbits in Group 1 set as normal. In the ischemia group (Group 2), 20 rabbits were made to suffer form ischemia for 4, 6, 8 and 10 hours respectively, with 5 at each time point. In the reperfusion group (Group 3), 55 rabbits were divided into 11 subgroups equally, and their left hind limbs were reperfused for 1, 3, 6, 12, 24, 72 hours and 1, 2, 4, 8, 12 weeks after 8 hours of ischemia. Superoxide dismutase (SOD), malondialdehyde (MDA), lactic acid and polymorphonuclear leukocyte (PMN) in the synovium were determined. At the same time, immunochemistry was employed to determine the factor vWF in order to count the capillaries. Results In the first 2 weeks of reperfusion, necrosis was the major change. Between 2 and 12 weeks, fibrosis and infiltration of PMN became more obvious with the capillaries decreasing, and the activity of the joint decreased in accordance with the destruction of the articular facet at this stage. SOD decreased significantly from 4 hours of ischemia to 8 weeks of reperfusion later, and MDA and PMN increased in the IR limbs than in the limbs in other groups. After 8 weeks of reperfusion, the capillaries in the IR limbs were significantly fewer than in the control limbs. Conclusions Ischemia-reperfusion of limbs can lead to obvious damage to the joint synovium. Destruction of the synovium, infiltration of PMN, dysfunction of blood supply and aggregation of metabolite may lead to the destruction of joint facet and thus acceleration of the progression of traumatic arthritis.