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我们在成功地复制出肝性脑病（ＨＥ）大白鼠模型的基础上，应用放射受体分析法对ＨＥ大鼠端脑、间脑、脑干和小脑的粗制突触体膜进行［￣３Ｈ］ＰＫ１１１９５受体结合分析，并设立对照组。结果表明，ＨＥ较对照鼠仅端脑和间脑的外周型苯二氮享受体（ＰＢＲ）结合位点数量显著增加（分别为Ｐ＜０．００１和Ｐ＜０．０５），以端脑尤甚；仅脑干ＰＢＲ亲和力升高（Ｐ＜０．０５）。提示ＨＥ发病与不同脑区ＰＢＲ改变导致的脑组织能量代谢障碍有关。本研究结果对于深入探讨ＨＥ发病机理和指导临床应用ＰＢＲ桔抗剂治疗ＨＥ具有一定意义
Based on the successful replication of HE model in rats, we used radionuclide analysis to study the synaptosomal membrane of the synapse in the telencephalon, diencephalon, brainstem and cerebellum of HE rats [~ 3H ] PK11195 receptor binding assay and set up a control group. The results showed that the number of peripheral benzodiazepine receptor (PBR) binding sites in HE and control group were significantly increased (P <0.001 and P <0.05, respectively) P <0.01). Only PBR affinity of brain stem increased (P <0.05). It suggests that the pathogenesis of HE is related to the disturbance of energy metabolism of brain tissue caused by the changes of PBR in different brain regions. The results of this study is of great significance to further explore the pathogenesis of HE and to guide the clinical application of PBR antagonist in the treatment of HE