Pathophysiology of Portal Hypertension, What's New?.
10.4166/kjg.2010.56.3.129
- Author:
Moon Young KIM
1
;
Soon Koo BAIK
Author Information
1. Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea. baiksk@medimail.co.kr
- Publication Type:Review ; English Abstract
- Keywords:
Portal hypertension;
Hepatic stellate cell;
Endothelial cell;
Intrahepatic vascular resistance
- MeSH:
Collateral Circulation/physiology;
Endothelial Cells/metabolism;
Hepatic Stellate Cells/metabolism;
Humans;
Hypertension, Portal/*etiology;
Liver Circulation/physiology;
Vascular Resistance
- From:The Korean Journal of Gastroenterology
2010;56(3):129-134
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Portal hypertension (PHT) is associated with changes in the intrahepatic, systemic and portosystemic collateral circulations. Alteration in vasoreactivity (vasodilation and vasoconstriction) plays a central role in the pathogenesis of PHT by contributing to increased intrahepatic resistance, hyperdynamic circulation and the expansion of the collateral circulation. PHT is also importantly characterized by changes in vascular structure; termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the sprouting of new blood vessels, also occurs in PHT, especially in the expansion of the portosystemic collateral circulation. These complementary processes of vasoreactivity, vascular remodeling and angiogenesis represent important targets in the research for the treatment of portal hypertension.