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目的：探讨程序性细胞死亡在缺血再灌注肌肉损伤中的作用及缺血再灌注肌肉损伤的发生机制。方法：运用末端脱氧核糖转移酶介导的生物素化脱氧尿嘧啶缺刻标记技术（ＴＵＮＥＬ）观察止血带致大鼠右后肢缺血再灌注腓肠肌细胞程序性死亡的特征与规律，并以左后肢作自身正常对照。结果：正常肌肉肌细胞完整，无程序性死亡细胞；再灌注４小时，肌细胞深度蓝染，程序性死亡细胞率为０．７０±０．０７；再灌注２４小时，肌细胞蓝染程度减轻，其程序性死亡细胞率为０．４８±０．０８，与再灌注４小时比较有极显著性差异（Ｐ＜０．０１）；再灌注２４小时，重度程序性死亡细胞率为０．１２±０．０８，与再灌注４小时（０．３６±０．０９）比较有极显著性差异（Ｐ＜０．０１）。结论：缺血再灌注能致肌肉细胞发生程序性死亡，以再灌注４小时最重，再灌注２４小时较４小时明显缓解
Objective: To investigate the role of programmed cell death in muscle injury induced by ischemia-reperfusion and the mechanism of muscle injury during ischemia-reperfusion. Methods: The terminal deoxyribo-transferase-mediated biotinylated deoxyuracil nick labeling (TUNEL) was used to observe the characteristics and regularity of programmed death of gastrocnemius cells in right hindlimb ischemia-reperfusion rats induced by tourniquet. Self-control. Results: Normal muscle cells were intact with no programmed cell death. Four hours after reperfusion, the muscle cells were deeply blue-stained and the rate of programmed cell death was 0.70 ± 0.07. After reperfusion for 24 hours, the degree of blue staining of muscle cells was reduced , The rate of programmed cell death was 0.48 ± 0.08, which was significantly different from that of 4h after reperfusion (P <0.01). The rate of severe programmed cell death was 0.12 ± 0.08, compared with 4 hours after reperfusion (0.36 ± 0.09), there was a significant difference (P <0.01). CONCLUSION: Ischemia-reperfusion can cause programmed cell death in muscle cells, which is most severe at 4 hours after reperfusion, significantly relieved at 4 hours after reperfusion