| Dokumentenart: | Artikel | ||||
|---|---|---|---|---|---|
| Titel eines Journals oder einer Zeitschrift: | American Journal of Physiology-Gastrointestinal and Liver Physiology | ||||
| Verlag: | AMER PHYSIOLOGICAL SOC | ||||
| Ort der Veröffentlichung: | BETHESDA | ||||
| Band: | 297 | ||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 4 | ||||
| Seitenbereich: | G849-G857 | ||||
| Datum: | 2009 | ||||
| Institutionen: | Medizin > Lehrstuhl für Innere Medizin I Medizin > Lehrstuhl für Innere Medizin II Medizin > Lehrstuhl für Pathologie | ||||
| Identifikationsnummer: |
| ||||
| Stichwörter / Keywords: | ENDOTHELIAL GROWTH-FACTOR; INTERNAL ELASTIC LAMINA; NITRIC-OXIDE SYNTHASE; CIRRHOTIC RATS; BACTERIAL TRANSLOCATION; BLOOD-FLOW; IN-VIVO; INCREASED ANGIOGENESIS; CAROTID-ARTERY; PRESSURE; mesenteric arteries; vasodilation | ||||
| Dewey-Dezimal-Klassifikation: | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin | ||||
| Status: | Veröffentlicht | ||||
| Begutachtet: | Ja, diese Version wurde begutachtet | ||||
| An der Universität Regensburg entstanden: | Ja | ||||
| Dokumenten-ID: | 66852 |
Web of ScienceZusammenfassung
Resch M, Wiest R, Moleda L, Fredersdorf S, Stoelcker B, Schroeder JA, Scholmerich J, Endemann DH. Alterations in mechanical properties of mesenteric resistance arteries in experimental portal hypertension. Am J Physiol Gastrointest Liver Physiol 297: G849-G857, 2009. First published August 20, 2009; doi: 10.1152/ajpgi.00084.2009.-Splanchnic vasodilation is the pathophysiological hallmark in the ...
Zusammenfassung
Resch M, Wiest R, Moleda L, Fredersdorf S, Stoelcker B, Schroeder JA, Scholmerich J, Endemann DH. Alterations in mechanical properties of mesenteric resistance arteries in experimental portal hypertension. Am J Physiol Gastrointest Liver Physiol 297: G849-G857, 2009. First published August 20, 2009; doi: 10.1152/ajpgi.00084.2009.-Splanchnic vasodilation is the pathophysiological hallmark in the development of the hyperdynamic circulatory syndrome in liver cirrhosis and portal hypertension. This has been attributed so far mainly to a marked vascular hyporeactivity to endogenous vasoconstrictors. However, myogenic tone and vessel stiffness have not been addressed in mesenteric arteries in liver cirrhosis. CCl4--induced ascitic cirrhotic (LC) and age-matched control rats, portal vein-ligated (PVL) rats, and sham-operated rats were investigated. Third-order mesenteric resistance arteries were studied under no-flow conditions using a pressure myograph measuring media thickness and lumen diameter in response to incremental increases in intramural pressure, from which wall mechanics were calculated. Electron microscopy was used for investigation of wall ultrastructure, especially the fenestrae in internal elastic lamina (IEL). In PVL animals, no significant change in passive vessel strain, stress, media-to-lumen ratio, or cross-sectional area was noted. In contrast, in LC rats, vessel strain was markedly elevated compared with healthy control rats, indicating a marked reduction in vessel stiffness. In addition, the strain-stress curve was shifted to the right, and the elastic modulus in dependency on vessel stress decreased, demonstrating predominantly structure-dependent factors to be involved. The media-to-lumen quotient was not significantly altered, but cross-sectional area was highly increased in LC rats, indicating hypertrophic outward remodeling. These findings were paralleled by enlarged fenestrae in the IEL but no change in thickness of IEL or proportion of extracellular matrix or vascular smooth muscle in LC rats. We concluded that, in long-standing severe portal hypertension such as ascitic LC but not in short-term conditions such as PVL, mesenteric resistance arteries exhibit vascular remodeling and markedly less resistant mechanical properties, leading to decreased vessel stiffness accompanied by structural changes in the IEL. This may well contribute to the maintenance and severity of splanchnic arterial vasodilation in LC.
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