Abstract
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. Key words: Reperfusion injury; Portal blood stasis; Endotoxin; Nuclear factor-κB
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