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目的：探讨缺血预处理（ＩＰＣ）对肝脏缺血再灌注损伤的保护作用及其机理。方法：采用大鼠部分肝脏原位缺血再灌注损伤模型，随机分成：①正常对照组，不作肝门阻断；②再灌注对照组：进行４５ ｍ ｉｎ 的肝门阻断及６０ ｍ ｉｎ 的再灌注；③预处理组：４５ ｍ ｉｎ 的肝门阻断前先进行５ ｍ ｉｎ 肝脏缺血及５ ｍ ｉｎ再灌注。②、③组均在６０ ｍ ｉｎ 再灌注完成后取血及肝组织标本检测肝功、ＮＯ、超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）及肝组织病理改变。结果：预处理组与再灌注对照组比较，肝功能明显改善，ＳＯＤ、ＮＯ 含量升高，ＭＤＡ 明显降低，两组比较差异显著。结论：缺血预处理对肝脏缺血再灌注损伤有明显保护作用，可能与提高内源性ＮＯ水平、清除氧自由基抑制脂质过氧化反应有关
Objective: To investigate the protective effect of ischemic preconditioning (IPC) on hepatic ischemia-reperfusion injury and its mechanism. Methods: The rat model of orthotopic liver ischemia-reperfusion injury was randomly divided into: ① normal control group, without hepatic portal block; ② reperfusion control group: 45-minute hepatic portal block and 60-minute Reperfusion; ③ Preconditioning group: The hepatic portal at 45 mm in diameter was occluded for 5 min before ischemia and then reperfused for 5 min. The blood and liver tissue samples were collected for liver function, NO, superoxide dismutase (SOD), malondialdehyde (MDA) and pathological changes of liver tissue after 60 min of reperfusion. Results: Compared with the reperfusion control group, the liver function of the pretreatment group was significantly improved, the content of SOD and NO increased, while the MDA decreased significantly. There was significant difference between the two groups. CONCLUSION: Ischemia preconditioning has a significant protective effect on hepatic ischemia-reperfusion injury, which may be related to the increase of endogenous NO level and scavenging oxygen free radicals to inhibit lipid peroxidation