缺血预处理对肝脏缺血再灌注损伤中MPO、TNF-α、ET、NO的影响

目的：探讨缺血预处理（IPC）对肝脏缺血再灌注（I/R）损伤中的中性粒细胞和某些细胞因子的影响。方法：采用大鼠部分肝脏原位缺血再灌注损伤模型，30只Wistar大鼠随机分成：①正常对照组；②缺血再灌注对照组；③预处理组。②、③组均在60min再灌注完成后取血及肝组织标本，检测血清AST、ALT、LDH、NO、ET-1、TNF-α、及肝组织中髓过氧化酶（MPO）活性和肝细胞病理改变。结果：预处理组与再灌注对照组比较，肝功明显改善，NO含量升高，ET-1、TNF-α浓度和MPO活性明显降低，两组比较差异具有显著性。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、减轻中性粒细胞在肝脏中的渗出和聚集、抑制ET-1、TNF-α的合成有关。

Effects of ischemic preconditioning on MPO, TNF-a, ET and NO in liver ischemia reperfusion injury

Objective To study effects of ischemic preconditioning (IPC) on polymorphonuclear neutrophils (PMN) and some cytokines during ischemia/reperfusion (I/R) injury in rats. Methods After the model of in situ hepatic I/R injury was established in 30 rats, the rats were randomized into the normal control group (N group), I/R group and ICP group. AST, ALT and LDH activities and nitric oxide (NO), endothelin (ET) and tumor necrosis factor (TNF) contents in serum, MPO activity in liver tissue and hepatic pathological changes were determined when 60-min reperfusion was completed in I/R and ICP groups. Results The values of AST, ALT and LDH, contents of ET and TNF, MPO activity were significantly lower but NO content higher in IPC group than in I/R group. Conclusion IPC may protect I/R injury by raising the endogenous NO level, relieving extravasation and aggregation of PMN in the liver and restraining synthesis of ET and TNF.