Regulation of Sinusoidal Perfusion in Portal Hypertension
β Scribed by Hendrik Reynaert; Daniel Urbain; Albert Geerts
- Book ID
- 101603408
- Publisher
- Wiley (John Wiley & Sons)
- Year
- 2008
- Tongue
- English
- Weight
- 79 KB
- Volume
- 291
- Category
- Article
- ISSN
- 1932-8486
- DOI
- 10.1002/ar.20669
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β¦ Synopsis
Abstract
Portal hypertension, a major complication of cirrhosis, is caused by both increased portal blood flow and augmented intrahepatic vascular resistance. Even though the latter is primarily caused by anatomical changes, it has become clear that dynamic factors contribute to the increased hepatic vascular resistance. The hepatic sinusoid is the narrowest vascular structure within the liver and is the principal site of blood flow regulation. The anatomical location of hepatic stellate cells, which embrace the sinusoids, provides a favorable arrangement for sinusoidal constriction, and for control of sinusoidal vascular tone and blood flow. Hepatic stellate cells possess the essential contractile apparatus for cell contraction and relaxation. Moreover, the mechanisms of stellate cell contraction are better understood, and many substances which influence contractility have been identified, providing a rationale and opportunity for targeting these cells in the treatment of portal hypertension in cirrhosis. Anat Rec, 291:693β698, 2008. Β© 2008 WileyβLiss, Inc.
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The mechanisms that regulate vascular resistance in the liver are an area of active investigation. Previously, we have shown that nitric oxide (NO) modulates hepatic vascular tone in the normal rat liver. In this study, the production of NO is examined in further detail by isolating sinusoidal endot