Hepatic ischemia‒reperfusion injury (HIRI) is a common and inevitable complication of hepatic trauma, liver resection, or liver transplantation. It contributes to postoperative organ failure or tissue rejection, eventually affecting patient prognosis and overall survival. The pathological mechanism of HIRI is highly complex and has not yet been fully elucidated. The proposed underlying mechanisms include mitochondrial damage, oxidative stress imbalance, abnormal cell death, immune cell hyperactivation, intracellular inflammatory disorders and other complex events. In addition to serious clinical limitations, available antagonistic drugs and specific treatment regimens are still lacking. Therefore, there is an urgent need to not only clarify the exact etiology of HIRI but also reveal the possible reactions and bottlenecks of existing drugs, helping to reduce morbidity and shorten hospitalizations. We analyzed the possible underlying mechanism of HIRI, discussed various outcomes among different animal models and explored neglected potential therapeutic strategies for HIRI treatment. By thoroughly reviewing and analyzing the literature on HIRI, we gained a comprehensive understanding of the current research status in related fields and identified valuable references for future clinical and scientific investigations.
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Background / Aim : The lipo-PGE1, known for being more stable during pulmonary circulation and having more targeting effect, has been reported to inhabit ET-1 induced stellate cell contraction. We assessed the effect of lipo-PGE1 on the change of ET-1 concentration and the relationship between ET-1 concentration and the liver damage. Methods : Mongrel dogs weighting about 25kg were divided into a control(n=6) and a lipo-PGE1 (n=6)group. Partial liver allotransplantation was performed. In the lipo-PGE1 group, lipo-PGE1 was slowly infused (60 ㎍/day) for 48 hours after reperfusion. The AST,ALP,LDH and ET-1 concentrations were monitored Results : The AST and ALP levels of the lipo-PGE1 group were significantly lower than those of the control group both at 1 hour and 48 hours after reperfusion. The LDH level in the lipo-PGE1 group was lower at 1 hour and 48 hours after reperfusion. But there was no statistical difference between the two groups. The baseline ET-1 concentration was elevated gradually in the control group. There was no significant difference between the two groups at 48 hours. There was no correlation between ET-1 concentrations and AST , ALP,LDH levels. Conclusion : This study demonstrated the hepatoprotective effect of the lipo-PGE1 against ischemia-reperfusion injury in canine partial liver allotransplantation. However, the baseline ET-1 level was eight tomes higher in the lipo-PGE1 group than that of the comntrol group in spite of the hepatoprotective effects of the lipo-PGE1. (Korean J Hepatol 2001;7 :475- 484)