Vascular endothelial dysfunction in cirrhosis

被引：280

作者：

Iwakiri, Yasuko

Groszmann, Roberto J. ^{[1
]}

机构：

[1] VA Connecticut Healthcare Syst, Hepat Hemodynam Lab, West Haven, CT USA

[2] Yale Univ, Sch Med, Sect Digest Dis, New Haven, CT USA

来源：

JOURNAL OF HEPATOLOGY | 2007年 / 46卷 / 05期

关键词：

D O I：

10.1016/j.jhep.2007.02.006

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Endothelial dysfunction is regarded as an early key event in multiple diseases. The assessment of vascular nitric oxide (NO) level is an indicative of endothelial dysfunction. In liver cirrhosis, on one hand, endothelial dysfunction is known as impaired endothelium-dependent relaxation in the liver microcirculation and contributes to increased intra-hepatic vascular resistance, leading to portal hypertension. On the other, increased production of vasodilator molecules mainly NO contributes to increased endothelium-dependent relaxation in the arteries of the systemic and splanchnic circulation. The aims of this review are to summarize and discuss: (1) unique characteristics of sinusoidal endothelial cell (SECs) and SEC dysfunctions in cirrhosis, and (2) endothelial dysfunctions in the arterial splanchnic and systemic circulation in cirrhosis with portal hypertension. (C) 2007 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

引用

页码：927 / 934

页数：8

共 92 条

[1]

Mild increases in portal pressure upregulate vascular endothelial growth factor and endothelial nitric oxide synthase in the intestinal microcirculatory bed, leading to a hyperdynamic state [J].