去除门静脉淤血减轻肝脏缺血再灌注损伤的实验研究

目的 探讨去除门静脉淤血对肝脏缺血再灌注损伤的影响及机制.方法 检测家兔肝脏原位冷灌注20、30、40 min后淤血的门静脉中内毒素含量变化,观察门静脉淤血去除对恢复灌流后4 h血清内毒素、丙氨酸转氨酶(ALT)、透明质酸(HA)、肝组织匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)及肝组织核因子-κB(NF-κB)活性的影响.结果 门静脉淤血中内毒素含量随阻断时间延长明显升高(P＜0.01),同一阻断时间每去除2.5 ml淤血血清内毒素含量显著下降(P＜0.01).在阻断30 min和40 min组,去除门静脉淤血能降低血清ALT、HA、及肝组织匀浆MDA的含量和肝组织NF-κB活性,增加肝组织匀浆SOD活性,与不去除相比较差异有统计学意义(P＜0.05).在阻断20 min组去除门静脉淤血与不去除相比较,各检测指标差异无统计学意义(P＞0.05).结论 门静脉淤血中内毒素含量随阻断时间延长明显升高,可能是引起肝脏损伤的主要原因;去除门静脉淤血可以减轻肝脏的再灌注损伤,其机制可能与门静脉淤血去除减少内毒素吸收,进而降低肝组织NF-κB活化有关.

Experimental study on amelioration of hepatic ischemia reperfusion injury by portal congestion blood removal

Objective To investigate the effect of portal blood stasis removal on hepatic ischemia reperfusion injury and explore its mechanism.Methods A rabbit hepatic model in situ hypothermic irrigation for 20,30,40 minutes was established.The endotoxin content in portal blood stasis by an order of 2.5 ml removal was observed.The changes of serum endotoxin,alanine aminotransferase (ALT),hyaluronic acid (HA),content of malondialdehyde (MDA) and activity of superoxide dismutase (SOD),the activation of nuclear factor-κB (NF-κB) in liver were examined after reperfusion for 4 h.Results The endotoxin content in portal blood stasis was significantly increased by extension of portal vein blocking (P＜0.01).At the same time of portal vein blocking,the endotoxin content significantly decreased with each 2.5 ml blood removal (P＜0.01).In the group of 30 or 40 minutes portal vein blocking,removing portal blood stasis ameliorated endotoxemia and hepatic ischemia reperfusion injury as shown by serum endotoxin,ALT,HA as well as the amount of MDA,SOD,NF-κB in hepatic tissues (P＜0.05),while the differences were not remarkable in the group of 20 minutes (P＞0.05).Conclusion The level of serum endotoxin is increased by extension of portal vein blocking and high volume of endotoxin may be responsible for hepatic reperfusion injury.Removing portal blood stasis may protect hepatic ischemia reperfusion injury.The possible mechanism may be that portal blood stasis removal reduced endotoxin absorption to reduce the activation of NF-κB.