肝硬化大鼠内脏血管壁NOS分布的免疫组化研究  

Distribution of Nitric Oxide Synthase in Splanchnic Vessels of Cirrhotic Rats by Immunohistochemistry

作　　者：余金生[1] 梁扩寰[1] 田德安[1] 唐望先[2] 王天才[2] 

机构地区：[1]武汉同济医科大学同济医院消化内科,430030 [2]同济医科大学肝病研究所

出　　处：《胃肠病学》1999年第3期150-152,共3页Chinese Journal of Gastroenterology

基　　金：国家自然科学基金!39670348

摘　　要：目的：观察肝硬化门静脉高压大鼠内脏动、静脉血管壁一氧化氮合酶（ＮＯＳ）的分布及染色强度变化，探讨ＮＯ在门静脉高压形成机制中的作用。方法：采用免疫组化染色法，应用两种ＮＯＳ特异性抗体，分别观察内皮型（ｅＮＯＳ）和诱生型（ｉＮＯＳ）ＮＯＳ的变化特点，并结合计算机图象分析系统对染色强度进行量化处理。结果：肝硬化大鼠肠系膜上动脉（ＳＭＡ）ｉＮＯＳ和ｅＮＯＳ染色强度与对照组相比均显著增加（Ｐ＜０．０１），其中以ｅＮＯＳ增加更为明显。而两组门静脉（ＰＶ）ＮＯＳ染色强度则无明显差异（Ｐ＞０．０５）。肝硬化组ＳＭＡ的ＮＯＳ染色强度明显高于ＰＶ（Ｐ＜０．０５）。结论：ＮＯＳ在内脏血管表达增多，以及在ＳＭＡ的表达高于ＰＶ，提示ＮＯ可能主要通过扩张内脏动脉、增加内脏血流量而参与门静脉高压的形成。Background/Aims: To explore the role of nitric oxide in the pathogenesis of portal hypertension. Methods: By immunohistochemical method, nitric oxide synthase(NOS) distribution of splanchnic vessels was studied with antibodies specific for eNOS or iNOS while NOS staining intensity was analyzed by computer image system. Results: iNOS, especially eNOS staining intensities in superior mensentery artery(SMA) of cirrhotic rats were significantly increased in comparison with normal rats(p< 0.01). There was no difference in these NOS staining intensities in portal vein(PV) between the two groups(P>0.05). Moreover, NOS staining intensities in SMA were markedly higher than those in PV of cirrhotic group. Conclusions: There is a difference in NOS expression between arteries and veins. NO may participate in the pathogenesis of portal hypertension mainly via dilating the splanchnic artery to increase portal flow.

关 键 词：NOS 肝硬化 内脏 大鼠 PV 血管壁 门静脉高压 增加 扩张 形成机制 

分 类 号：R575.2[医药卫生—消化系统] R657.34[医药卫生—内科学]