HOLSTEGE, A and ANDUS, T and GROSS, V and KOLLINGER, M and SCHOLMERICH, J (1993) PATHOGENESIS OF PORTAL-HYPERTENSION. MEDIZINISCHE WELT, 44 (7). pp. 431-438. ISSN 0025-8512,
Full text not available from this repository.Abstract
According to Ohm's law, portal hypertension is characterized by an increased resistance of either prehepatic, hepatic or posthepatic blood vessels and an enhanced perfusion of the portal vein. The rise in portal blood flow is caused by a lowering of the resistance of splanchnic arteriolar vessels. The pathogenesis of the splanchnic hyperdynamic circulation is not completely understood although several potential mediators have been identified including nitric oxide, glucagon and adenosine. Hepatic sinusoidal resistance appears to be modulated by perisinusoidal cells located in the space of Disse. These cells cause a narrowing of the sinusoidal lumen when they are stimulated to contract upon exposure to various agents. Kupffer cells have been shown to release some of these mediators. Subsequent to their disease-associated transformation into myofibroblasts, perisinusoidal cells produce excessive amounts of collagen within the space of Disse. Accordingly, perisinusoidal cells are involved both in the reversible and in the irreversible increase in portal hepatic resistance observed in chronic liver diseases.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ; PORTAL HYPERTENSION; HYPERDYNAMIC CIRCULATION; VASOACTIVE COMPOUNDS; PATHOGENESIS |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:42 |
| URI: | https://pred.uni-regensburg.de/id/eprint/53903 |
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