Continuous infusion of N-acetylcysteine reduces liver warm ischaemia-reperfusion on injury
Continuous infusion of N-acetylcysteine reduces liver warm ischaemia-reperfusion on injury
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DOI：
10.1002/bjs.4694
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发表时间：
2004-10-01
影响因子：
9.6
通讯作者：
Davidson, BR
中科院分区：
文献类型：
--
作者：
Glantzounis, GK;Yang, W;Davidson, BR
背景资料：N-乙酰半胱氨酸（NAC）可以调节肝脏热缺血再灌注（IR）损伤的初始阶段（小于2小时），但其对晚期的影响尚不清楚。本研究探讨了NAC的作用，在早期和晚期阶段在兔叶IR model.Methods：肝缺血诱导流入闭塞的中位数和左肝叶60分钟，再灌注7小时。NAC组（n = 6）于再灌注前15 min静脉注射NAC 150 mg/kg，再灌注期间维持NAC 10 mg/kg/h。IR组（n = 6）在再灌注前15 min内持续输注5%葡萄糖20 ml，输注速率为10 ml/h。假手术组（n = 6）行开腹手术，但不造成肝脏缺血。结果：再灌注2 h后，NAC组细胞内氧合明显高于ER组（P = 0.023）。肝脏微循环在再灌注5 h后明显改善（P = 0.036），丙氨酸氨基转移酶活性（P = 0.007）和吲哚菁绿色清除率（摄取，P = 0.001;排泄，P = 0.032）在再灌注5 h后肝脏损伤明显减轻。
Background: N-acetylcysteine (NAC) may modulate the initial phase (less than 2 h) of liver warm ischaemia-reperfusion (IR) injury but its effect on the late phase remains unclear. The present study investigated the role of NAC during the early and late phases in a rabbit lobar IR model.Methods: Liver ischaemia was induced by inflow occlusion to the median and left liver lobes for 60 min, followed by 7 h of reperfusion. In the NAC group (n = 6), NAC was administered intravenously at 150 mg per kg over the 15 min before reperfusion and maintained at 10 mg per kg per h during reperfusion. In the IR group (n = 6), 20 ml 5 per cent dextrose was infused over the 15 min before reperfusion and continued at a rate of 10 ml/h. Animals in a sham operation group (n = 6) underwent laparotomy but no liver ischaemia. All animals were killed at the end of the experiment.Results: Intracellular tissue oxygenation was improved after the second hour of reperfusion in animals treated with NAC compared with that in the ER group (P = 0.023). Hepatic microcirculation improved after 5 h of reperfusion (P = 0.036) and liver injury was reduced after 5 h, as indicated by alanine aminotransferase activity (P = 0.007) and indocyanine green clearance (uptake, P = 0.001; excretion, P = 0.032).Conclusion: The main protective effect of NAC becomes apparent 5 h after hepatic ischaemic injury.