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为探讨肝脏缺血再灌注损伤过程中血小板激活因子（ｐｌａｔｅｌｅｔａｃｔｉｖａｔｉｎｇｆａｃｔｏｒ，ＰＡＦ）及中性粒细胞的作用及其机理，作者在建立大鼠肝脏局部缺血再灌注损伤模型的基础上，对ＰＡＦ的变化及中性粒细胞的浸润程度进行了初步研究，观察了ＰＡＦ拮抗剂海风藤酮对大鼠肝脏局部缺血再灌注损伤的保护作用。结果表明：肝脏缺血再灌注损伤时肝组织ＰＡＦ含量增高，且随再灌注时间的延长而加重；早期肝组织抗氧化能力下降，大量氧自由基生成，以及细胞内钙超载是损伤的主要原因，而肝脏Ⅱ相损伤主要是由于肝组织ＰＡＦ的积聚，激活中性粒细胞，导致溶酶体酶和毒性自由基的产生所致。海风藤酮可以拮抗损伤过程中ＰＡＦ增高所致的药理作用，减轻肝脏脂质过氧化程度，改善肝功能，减轻肝脏病变程度。本实验结果提示：ＰＡＦ拮抗剂可能为肝脏缺血再灌注损伤的防治提供一条新的途径
To investigate the role and mechanism of plateletactivating factor (PAF) and neutrophils in the process of hepatic ischemia-reperfusion injury, the authors established a hepatic model of hepatic ischemia-reperfusion injury in rats. The changes and neutrophil infiltration were preliminary studied. The protective effect of PAF antagonist sea rotenone on hepatic ischemia-reperfusion injury in rats was observed. The results showed that the hepatic PAF content increased during hepatic ischemia-reperfusion injury and increased with the prolongation of reperfusion time. The antioxidation ability of hepatic tissue in the early stage was decreased, a large number of oxygen free radicals were generated, and intracellular calcium overload was the main cause of injury. , And liver II phase damage is mainly due to the accumulation of PAF in liver tissue, activation of neutrophils, resulting in the production of lysosomal enzymes and toxic free radicals. Sea rotenone can antagonize the pharmacological effects caused by increased PAF during injury, reduce the degree of hepatic lipid peroxidation, improve liver function, and reduce liver lesions. The results of this experiment suggest that PAF antagonists may provide a new way for the prevention and treatment of hepatic ischemia-reperfusion injury.