Zhang Z M, Qiu F Z, Chen X P
Department of Surgery, Tongji Hospital, Tongji Medical University, Wuhan.
Zhonghua Yi Xue Za Zhi. 1994 Apr;74(4):238-40, 256.
We evaluated the effect of vasoactive intestinal peptide (VIP) receptor, a brain-gut peptide receptor, which is capable of exciting central neurons, on the pathogenesis of hepatic encephalopathy (HE). By means of radioligand binding assay, VIP receptors in crude synaptosomal membrane of rat brains were investigated in a rat model of HE induced by partial hepatectomy following carbon tetrachloride intoxication and in controls. A dissociation constant (Kd) was found 0.28 +/- 0.01 nmol/L and a maximal binding capacity (Bmax) 9.56 +/- 0.29 fmol/mg of protein in HE rats. Only decreased Bmax values were observed (P < 0.002) and the Kd values were statistically unchanged (P > 0.20) in HE rats as compared with in controls. The results suggest that the changes of VIP receptors in brains play a significant role in the pathogenesis of HE. The mechanism of HE induced by the alterations of VIP receptors in the brains was described.
我们评估了血管活性肠肽（VIP）受体（一种脑肠肽受体，能够兴奋中枢神经元）对肝性脑病（HE）发病机制的影响。通过放射性配体结合试验，在四氯化碳中毒后行部分肝切除术诱导的HE大鼠模型及对照大鼠中，研究了大鼠脑粗突触体膜中的VIP受体。在HE大鼠中，解离常数（Kd）为0.28±0.01 nmol/L，最大结合容量（Bmax）为9.56±0.29 fmol/mg蛋白质。与对照组相比，HE大鼠仅观察到Bmax值降低（P<0.002），而Kd值无统计学变化（P>0.20）。结果表明，脑中VIP受体的变化在HE发病机制中起重要作用。文中描述了脑内VIP受体改变诱导HE的机制。
