在正常大鼠和门静脉高压大鼠中可检测到内皮型一氧化氮合酶，但未检测到诱导型一氧化氮合酶。

Endothelial, but not the inducible, nitric oxide synthase is detectable in normal and portal hypertensive rats.

作者信息

Stumm Michael Martin, D'Orazio Daniel, Sumanovski Lazar Trajan, Martin Pierre-Yves, Reichen Juerg, Sieber Cornel Christian

机构信息

Department of Research, University Hospital Basel, 4031-Basel, Switzerland.

出版信息

Liver. 2002 Dec;22(6):441-50. doi: 10.1034/j.1600-0676.2002.01653.x.

DOI:10.1034/j.1600-0676.2002.01653.x

PMID:12445168

Abstract

BACKGROUND

Chronic portal hypertension is accompanied by a nitric oxide (NO) dependent vasodilation. Three isoforms of NO producing synthases (NOS) are characterized: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Sources of increased NO levels in chronic hypertension is disputed.

METHODS

To determine eNOS and iNOS expression in different organs of portal hypertensive and control rats, we divided Sprague-Dawley rats in 6 groups: (1). Partial portal vein ligated rats, (2). Bile duct ligated rats, (3). Carbon tetrachloride treated rats, (4). Sham operated rats, (5). Untreated control rats, and (6). LPS treated rats. Immunohistochemistry (IHC) and immunoblotting (IB) using antibodies against eNOS or iNOS were carried out on samples from thymus, aorta, heart, lung, oesophagus, liver, spleen, kidney, pancreas, small and large intestine.

RESULTS

IHC revealed an even eNOS expression in all groups. Expression of iNOS was restricted to macrophages in organs of LPS treated and the thymus of rats. IB mirrored these results.

CONCLUSION

In chronic portal hypertension, the main source for NO production depends on eNOS activity.

摘要

背景

慢性门静脉高压伴有一氧化氮（NO）依赖性血管舒张。已鉴定出三种产生NO的合酶（NOS）亚型：神经元型NOS（nNOS）、内皮型NOS（eNOS）和诱导型NOS（iNOS）。慢性高血压中NO水平升高的来源存在争议。

方法

为了确定门静脉高压大鼠和对照大鼠不同器官中eNOS和iNOS的表达，我们将斯普拉格-道利大鼠分为6组：（1）部分门静脉结扎大鼠，（2）胆管结扎大鼠，（3）四氯化碳处理大鼠，（4）假手术大鼠，（5）未处理的对照大鼠，以及（6）脂多糖处理大鼠。使用抗eNOS或iNOS抗体，对来自胸腺、主动脉、心脏、肺、食管、肝脏、脾脏、肾脏、胰腺、小肠和大肠的样本进行免疫组织化学（IHC）和免疫印迹（IB）分析。