Increased angiogenesis and permeability in the mesenteric microvasculature of rats with cirrhosis and portal hypertension:: an in vivo study
Increased angiogenesis and permeability in the mesenteric microvasculature of rats with cirrhosis and portal hypertension:: an in vivo study
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DOI：
10.1111/j.1478-3231.2006.01308.x
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发表时间：
2006-09-01
影响因子：
6.7
通讯作者：
Colle, Isabelle
中科院分区：
文献类型：
--
作者：
Geerts, Anja M.;De Vriese, An S.;Colle, Isabelle
背景：在门静脉高压症（PHT）和肝硬化的内脏血管扩张中缺乏血管生成的体内证据。血管内皮生长因子（VEGF）和内皮型一氧化氮合酶（eNOS）是血管生成的介质。本研究可视化在体内的结构变化（血管生成和血管通透性过高），并检查存在的血管内皮生长因子和eNOS在肠系膜微血管的PHT与肝硬化的动物模型。方法：采用部分门静脉结扎（PPVL）和胆总管结扎（CBDL）方法建立大鼠肝硬化模型。活体显微镜检查肠系膜微循环。免疫组化法检测肠系膜组织VEGF、eNOS和CD 31的表达。结果如下：活体显微镜和CD 31染色显示，与假手术组和对照组相比，PPVL和CBDL大鼠肠系膜血管生成增加。VEGF和eNOS在CBDL和PPVL大鼠中的表达均高于对照组，且与血管密度呈正相关。与对照组和PPVL大鼠相比，高分子渗漏在哮喘大鼠中增加。结论：我们的研究提供了体内证据，增加血管生成的肠系膜微血管的动物模型PHT和肝硬化。PPVL和CBDL大鼠肠系膜中VEGF和eNOS表达增加可能表明它们的贡献。肠系膜血管中的微血管通透性仅在痉挛大鼠中增加。
Background: In vivo evidence for angiogenesis in the splanchnic vasodilation in portal hypertension (PHT) and cirrhosis is lacking. Vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) are mediators of angiogenesis. The present study visualises in vivo structural changes (angiogenesis and vascular hyperpermeability) and examines the presence of VEGF and eNOS in the mesenteric microvasculature of animal models of PHT with and without cirrhosis. Methods: Portal hypertension was induced by partial portal vein ligation (PPVL) and cirrhosis was induced by common bile duct ligation (CBDL) in rats. The mesenteric microcirculation was examined by intravital microscopy. Expression of VEGF, eNOS and CD31 in mesenteric tissue were studied by immunohistochemistry. Results: An increased mesenteric angiogenesis was observed in PPVL and CBDL rats compared with Sham-operated and control rats, as shown by intravital microscopy and CD 31 staining. VEGF and eNOS expression was higher in CBDL and PPVL rats compared with control groups and correlated positively with vascular density. Macromolecular leakage was increased in cirrhotic rats compared with control and PPVL rats. Conclusion: Our study provides in vivo evidence of an increased angiogenesis in the mesenteric microvasculature of animal models of PHT and cirrhosis. Increased VEGF and eNOS expression in the mesentery of PPVL and CBDL rats may suggest their contribution. Microvascular permeability in the mesenteric vessels was only increased in cirrhotic rats.