血小板激活因子在肝脏缺血-再灌注损伤中的变化及山莨菪碱的保护作用

The role of plateletactivating factor in hepatic ischemiareperfusion injury and the protective effect of anisodamine

目的 :探讨血小板激活因子 (PAF)在肝脏缺血再灌注损伤中的意义及山莨菪碱的保护作用。方法 :测定大鼠肝脏局部缺血再灌注损伤和应用山莨菪碱时肝组织 PAF含量、丙二醛 (MDA)含量及肝脏病理变化。结果 :肝脏缺血再灌注损伤时肝组织 PAF含量增高 ,由 (2 2 7.72± 31.13) pg/ g升至 (4 6 7.16± 5 3.48) pg/ g,且随再灌注时间的延长而增高 ;山莨菪碱明显减少肝脏缺血再灌注损伤时肝组织 PAF的释放 ,减轻肝脏脂质过氧化程度 ,改善肝功能 ,减轻肝脏病变程度。结论 :山莨菪碱部分是通过抑制 PAF的产生而对肝脏缺血再灌注损伤起保护作用。

Objective:To study the role of plateletactivating factor (PAF) in hepatic ischemiareperfusion injury and the protective effects of anisodamine.Methods:Tissue PAF and malondialdehyde (MDA) contents were measured in rats with or without anisodamine treatment during hepatic ischemiareperfusion injury.The pathological change in hepatic tissue was also observed.Results:As the liver reperfusion prolonged,tissue PAF levels elevated from (227 72±31 13)pg/g to (467 16±53 48)pg/g. After intravenous administration of anisodamine,the release of PAF was remarkably decreased.Serum enzymes,MDA content and the degree of liver injury were significantly lower than those of untreated groups ( P <0 01).Conclusions:PAF may play an important role in liver ischemiareperfusion injury,and its deleterious effects can be blocked by treatment with anisodamine.