缺血预处理对骨骼肌再灌流损伤的保护作用

目的：探讨缺血预处理对肢体骨骼肌缺血再灌流损伤的保护作用．方法：选择２４只家兔，随机等分为实验组和对照组．用气囊止血带阻断家兔后肢血流造成缺血再灌流损伤模型，测定缺血期肌糖原吸光度及再灌流期血清中肌酸磷酸激酶（ＣＰＫ）、谷草转氨酶（ＡＳＴ）和乳酸脱氢酶（ＬＤＨ）含量，电镜下观察骨骼肌结构变化．结果：缺血４小时，实验组肌糖原吸光度显著高于对照组（Ｐ＜０．０５）．再灌流１、２小时，实验组血清中ＣＰＫ、ＡＳＴ和ＬＤＨ含量显著低于对照组（Ｐ＜０．０５）．实验组线粒体空泡变性和肌原纤维溶解程度轻于对照组．结论：缺血预处理能减慢肌糖原分解代谢速度，对骨骼肌缺血再灌流损伤有明显的保护作用．

Protective Effect of Ischemic Preconditioning on Reperfusion Injury of Skeletal Muscle in Limb

Aim: The purpose of this study is to explore the possibility to protect skeletal muscls in limb from ischemia and reperfusion injury with ischemic preconditioning. Methods: Twenty four healthy rabbits of either sex were selected and randomly divided into an ischemic preconditioned (experiment) group and a nonpreconditioned (control) group equally in this experiment. The model of ischemia and reperfusion injury was caused by blocking the blood flows of rabbit hind limbs with a pneumatic tourniquet. The photoabsorbance of muscle glycogen during ischemia and contents of creatine phosphate kinase (CPK), aspartate aminotransferase (AST) and lactic acid dehydrogenase (LDH) in the serum during reperfusion were measured respectively. Structural changes of the skeletal muscle were observed with an electron microscope. Results: The photoabsorbance of muscle glycogen in the experimental group was significantly higher than that in the control group at 4 hour of ischemia ( P <0.05). CPK, AST and LDH were lower in the experimental group than in the control group at 1 and 2 hours after reperfusion ( P <0.05). Compared with the control group, mitochondrial vacuolar degeneration and dissolution of the myofibril in the experimental group were significantly reduced and delayed. Conclusion: We deem that IPC decelerates glycogenolysis and remarkably protects skeletal muscle from ischemia and reperfusion injury.