Zhang Z, Qiu F
Department of Surgery, Tongji Hospital, Tongji Medical University, Wuhan.
Chin Med J (Engl). 1995 May;108(5):328-31.
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 radio-ligand binding assay, VIP receptors in the crude synaptosomal membranes of rat brains were investigated in rat models with HE induced by partial hepatectomy following carbon tetrachloride intoxication and in controls. The binding to the VIP receptor was studied, with 125I-VIP as a radioligand. Scatchard analysis of the binding data was linear, yielding a dissociation constant (Kd) of 0.28 +/- 0.01 nM and a maximal binding capacity (Bmax) of 9.56 +/- 0.29 fmol/mg of protein in HE rats. Only decreased Bmax values were observed (P < 0.002), while the Kd values were statistically unchanged (P > 0.20) in HE rats as compared with the controls. The results suggest that the changes of VIP receptors in the brains of HE rats play a significant role in the pathogenesis of HE. The mechanism of HE induced by the alterations of VIP receptors in the brains was discussed.
我们评估了血管活性肠肽(VIP)受体(一种能够兴奋中枢神经元的脑肠肽受体)对肝性脑病(HE)发病机制的影响。通过放射性配体结合测定法,在四氯化碳中毒后行部分肝切除术诱导的HE大鼠模型及对照组中,研究大鼠脑粗突触体膜中的VIP受体。以125I-VIP作为放射性配体研究其与VIP受体的结合。对结合数据进行Scatchard分析呈线性,在HE大鼠中解离常数(Kd)为0.28±0.01 nM,最大结合容量(Bmax)为9.56±0.29 fmol/mg蛋白质。与对照组相比,在HE大鼠中仅观察到Bmax值降低(P<0.002),而Kd值无统计学变化(P>0.20)。结果提示,HE大鼠脑中VIP受体的变化在HE发病机制中起重要作用。并讨论了脑内VIP受体改变诱导HE的机制。