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目的探讨α肾上腺素受体亚型拮抗剂和钙通道阻滞剂对门静脉的作用机制及其在肝硬变门脉高压情况下的变化．方法采用药物受体分析技术，结合离体和整体实验，进行肝硬变门脉高压鼠和正常鼠的对照研究．分析测定了：①哌唑秦（ｐｒａｚｏｓｉｎｅ，Ｐｒａ），育亨宾（ｙｏｈｉｍｂｉｎｅ，Ｙｏｈ），硝苯吡啶（ｎｉｆｒｄｉｐｉｎｅ，Ｎｉｆ）与门静脉α受体的亲和力，②Ｐｒａ，Ｙｏｈ，Ｎｉｆ对门静脉收缩效应的影响；Ｐｒａ和Ｎｉｆ对门静脉压力的影响．结果正常鼠门静脉对Ｐｒａ的亲和力为Ｙｏｈ１２８倍，而ＰＨＴ鼠二者却相差不显著（Ｐ＞００５），其中对Ｐｒａ的亲和力下降了５倍，Ｙｏｈ增加了２７７倍．对Ｎｉｆ的亲和力正常鼠为ＰＨＴ鼠的１４倍．Ｐｒａ和Ｎｉｆ使门静脉收缩曲线显著右移，对门静脉收缩效应的抑制率分别为：对照组，Ｐｒａ７１２％，Ｎｉｆ８９９％，ＰＨＴ组，Ｐｒａ６８２％，Ｎｉｆ７４４％．Ｐｒａ能显著降低两组鼠的门静脉压力，Ｎｉｆ显著降低正常鼠的门静脉的压力，而ＰＨＴ鼠仅轻度下降（Ｐ＞００５）．结论门静脉突触后α受体亚型是α１，而α１的亚型主要是α１ａ，Ｐｒａ和Ｎｉｆ通过阻断α１和α１ａ受体而抑制门静脉收缩，降低门静脉压力．因此α?
Objective To investigate the effect of α-adrenergic receptor subtype antagonist and calcium channel blocker on portal vein and its changes in cirrhotic patients with portal hypertension. Methods Drug receptor analysis techniques, combined with in vitro and in vivo experiments, the control study of cirrhotic patients with portal hypertension and normal mice. The effects of prazosine (Pra), yohimbine (Yoh), nifrdipine (Nif) on the portal vein α receptor and the effects of Pra, Yoh and Nif on the contraction of the portal vein were analyzed. ; Pra and Nif on the portal pressure. Results The normal mouse portal vein had a Yh128 fold affinity for Pra, whereas the PHT mice showed no significant difference (P> 005). The affinity for Pra decreased 5-fold and Yoh increased 27.7-fold. Fetal affinity for Nif is 14 times that of PHT mice. Pra and Nif significantly right portal vein contraction curve, the inhibitory effect of portal vein contractile effect were: the control group, Pra71 2%, Nif89 9%, PHT group, Pra68 2%, Nif74 4%. Pra significantly reduced portal pressure in both groups. Nif significantly reduced portal pressure in normal mice, while PHT decreased only slightly (P> 005). Conclusions Post-synaptic alpha receptor subtypes are α1 and α1 subtypes are mainly α1a. Pra and Nif inhibit portal vein contractility and decrease portal pressure by blocking α1 and α1a receptors. So α?