门静脉高压症大鼠内脏血管壁上血管紧张素Ⅱ受体的变化  

CHANGES OF SPLANCHNIC VASCULAR ANGIOTENSIN Ⅱ RECEPTORS IN RATS WITH PORTAL HYPERTENSION

作　　者：李继坤[1,2,3] 戴植本[1,2,3] 崔武任 

机构地区：[1]上海市第一人民医院外科 [2]同济医科大学同济医院外科 [3]同济医科大学核医学研究室

出　　处：《中国普外基础与临床杂志》1998年第3期140-142,共3页Chinese Journal of Bases and Clinics In General Surgery

摘　　要：为探讨门静脉高压症（ＰＨＴ）内脏高动力循环的发生机理，我们采用放射配基结合分析法检测肝前型ＰＨＴ大鼠内脏血管壁上血管紧张素Ⅱ（ＡⅡ）受体的最大结合容量（Ｂｍａｘ）和平衡解离常数（Ｋｄ）变化。结果：ＰＨＴ组（ｎ＝２０）肠系膜上动脉和门静脉壁上ＡⅡ受体的Ｂｍａｘ（分别为２０６．９±３９．３ｆｍｏｌ／ｍｇ蛋白和３１．５±９．２ｆｍｏｌ／ｍｇ蛋白）较对照组（ＳＯ，ｎ＝１６，分别为２９７．２±４４．７ｆｍｏｌ／ｍｇ蛋白和５３．４±１２．１ｆｍｏｌ／ｍｇ蛋白）明显降低（Ｐ＜０．０１）；肠系膜上动脉的Ｋｄ值（１．０３±０．１１ｎｍｏｌ／Ｌ）较ＳＯ组（０．８８±０．０８ｎｍｏｌ／Ｌ）明显升高（Ｐ＜０．０５），门静脉的Ｋｄ值虽较ＳＯ组略有升高，但无统计学意义。本实验结果表明，ＰＨＴ大鼠内脏血管对ＡⅡ反应性下降的原因之一在于血管壁上ＡⅡ受体的数量减少和亲和力下降，从而对高动力循环形成起一定的介导作用。To investigate the mechanisms of splanchnic hyperdynamics in portal hypertension (PHT), angiotensin Ⅱ (A Ⅱ) receptor maximal binding capacity (Bmax) and dissociation constants (Kd) of splanchnic blood vessels in rats with prehepatic PHT were studied by radioligand binding analysis. The results showed that the A Ⅱ receptor Bmax in the superior mesenteric artery and portal vein of PHT animals (206.9±39.3 fmol/mg protein and 31.5±9.2 fmol/mg protein respectively) was all significantly lower than that of the controls (297.2±44.7 fmol/mg protein and 53.4±12.1 fmol/mg protein respectively, P <0.01). The A Ⅱ receptor Kd in the superior mesenteric artery was markedly increased in PHT animals (1.03± 0.11 nmol/L) compared with that in controls (0.88±0.08 nmol/L, P <0.05). In the portal vein, the A Ⅱ receptor Kd in PHT animals was slightly higher than in controls, but no significant difference was observed between the two groups. These results suggest that the vascular hyporesponsiveness to A Ⅱ in PHT is caused partially by a reduction in number and a decrease in affinity of vascular A Ⅱ receptors, and these changes may possibly lead to the formation of hyperdynamic circulation.

关 键 词：门静脉高压 血管紧张素Ⅱ 受体 放射配位体测定 

分 类 号：R657.34[医药卫生—外科学]