Publication
Title
Hemodynamic changes in splanchnic blood vessels in portal hypertension
Author
Abstract
Portal hypertension (PHT) is associated with a hyperdynamic state characterized by a high cardiac output, increased total blood volume, and a decreased splanchnic vascular resistance. This splanchnic vasodilation is a result of an important increase in local and systemic vasodilators (nitric oxide, carbon monoxide, prostacyclin, endocannabinoids, and so on), the presence of a splanchnic vascular hyporesponsiveness toward vaso-constrictors, and the development of mesenteric angiogenesis. All these mechanisms will be discussed in this review. To decompress the portal circulation in PHT, portosystemic collaterals will develop. The presence of these portosystemic shunts are responsible for major complications of PHT, namely bleeding from gastrointestinal varices, encephalopathy, and sepsis. Until recently, it was accepted that the formation of collaterals was due to opening of preexisting vascular channels, however, recent data suggest also the role of vascular remodeling and angiogenesis. These points are also discussed in detail.
Language
English
Source (journal)
The anatomical record: advances in integrative anatomy and evolutionary biology. - New York, N.Y.
Publication
Hoboken : Wiley , 2008
ISSN
1932-8486 [print]
1932-8494 [online]
DOI
10.1002/AR.20667
Volume/pages
291 :6 (2008) , p. 699-713
ISI
000256718800011
Pubmed ID
18484617
Full text (Publisher's DOI)
UAntwerpen
Research group
Publication type
Subject
External links
Web of Science
Record
Identifier
Creation 15.02.2024
Last edited 16.02.2024
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