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采用低流率-再灌流模型研究脂质过氧化在再灌流性肝损伤中的作用,肝脏经过90min低速率灌流未见明显损伤,当灌流速率恢复到正常后中心静脉周围区(PC区)细胞发生迅速不可逆损害,并伴有丙二醛生成率大幅度上升,低速率灌流期间,灌流液中黄嘌呤与次黄嘌吟浓度由原来的1.5和3.6μmol·L~(-1)逐步升高至5.5和11.5μmol·L~(-1),自由基清除剂儿茶酸能使再灌流期丙二醛生成率由295 nm01·g~(-1)·h~(-1)下降至109 nmol·g~(-1)·h~(-1),并使LDH释放率减少约50％,PC区细胞死亡率减少89％,再灌流初期用氮饱和灌流液冲洗3 min,使再灌流所致的LDH释放下降约50％,PC区细胞死亡率减少84％,别嘌吟醇(2～6mmol·L~(-1))对防止再灌流性肝损伤表现出明显的剂量效应关系。 与预计结果相反低浓度别嘌呤醇(0.5～1mmol·~(-1))能增加再灌流性肝损伤,400μmol·L~(-1)黄嘌呤则使再灌流性肝损伤明显减轻,其代谢产物尿酸对降低再灌流时丙二醛生成率以及细胞损害均表现出明显的剂量反应关系。
Low perfusion-reperfusion model was used to study the role of lipid peroxidation in reperfusion-induced liver injury. No obvious damage was observed in the liver after a 90-min perfusion. When the perfusion rate returned to normal, cells in the central venous zone (PC) Rapid and irreversible damage, accompanied by a significant increase in the rate of formation of malondialdehyde. During the low-rate perfusion, the concentration of xanthine and hypoxanthine in the perfusate gradually increased from 1.5 and 3.6 μmol·L -1 To 5.5 and 11.5μmol·L -1, the free radical scavenger catechin decreased the malondialdehyde formation rate from 295 nm · · -1 · h -1 to 109 nmol · g -1 · h -1, and the release rate of LDH was reduced by about 50%. The cell death rate in PC area was reduced by 89%. After initial perfusion, the cells were washed with nitrogen saturated perfusate for 3 min, Induced LDH release decreased by about 50%, PC area cell death rate decreased by 84%, allopurinol (2 ~ 6mmol·L -1) on the prevention of reperfusion liver injury showed a significant dose-response relationship. In contrast, low concentrations of allopurinol (0.5 ~ 1 mmol ·· -1) increased the reperfusion injury of liver and the 400 μmol·L -1 xanthine significantly reduced the reperfusion injury, and the metabolism Product uric acid showed a dose-response relationship with decreasing the malondialdehyde (MDA) production rate and cell damage during reperfusion.