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采用大鼠肝缺血再灌注损伤模型，放免法检测缺血后、缺血再灌注２小时和缺血再灌注２４小时３个时限肝组织血栓素Ｂ２与６－酮－前列腺素Ｆ１α含量，并作血清酶测定、光镜及电镜检查，探讨血栓素Ａ２、前列环素在肝缺血再灌注损伤中的作用及中药制剂川芎嗪的影响。结果：肝缺血再灌注时肝组织血栓素Ｂ２含量明显升高（Ｐ＜０．０５），以再灌注早期为著（Ｐ＜０．０１），６－酮－前列腺素Ｆ１α含量虽也升高，但差异无显著性（Ｐ＞０．０５）。应用川芎嗪后缺血肝组织血栓素Ｂ２含量明显降低（Ｐ＜０．０５），病理损伤亦较轻。提示：血栓素Ａ２、前列环素这对微循环调节因子的代谢失衡是参与肝缺血再灌注损伤发生的重要因素之一，川芎嗪可对抗血栓素Ａ２的合成与活性，从而减轻肝缺血再灌注损伤。
The model of hepatic ischemia / reperfusion injury in rats was established. The levels of thromboxane B2 and 6-keto-PGF1α in liver tissues were detected by radioimmunoassay three hours after ischemia, 2 hours after ischemia-reperfusion and 24 hours after ischemia-reperfusion Serum enzyme assay, light microscopy and electron microscopy to explore the role of thromboxane A2, prostacyclin in liver ischemia-reperfusion injury and the impact of Chinese medicine preparation of ligustrazine. Results: The content of thromboxane B2 in hepatic tissue was significantly increased (P <0.05) during the period of hepatic ischemia-reperfusion, and the content of 6-keto-prostaglandin F1α was also increased at the early stage of reperfusion High, but the difference was not significant (P> 0.05). The thromboxane B2 content of ischemic liver tissue was significantly reduced (P <0.05) after application of ligustrazine, and pathological injury was also lighter. It is suggested that the metabolic imbalance of thromboxane A2 and prostacyclin on the microcirculation regulators is one of the important factors involved in the occurrence of hepatic ischemia-reperfusion injury. Tetramethylpyrazine can antagonize the synthesis and activity of thromboxane A2 and thus reduce the hepatic ischemia Reperfusion injury.