Endothelial nitric oxide synthase is not essential for the development of fibrosis and portal hypertension in bile duct ligated mice
| Autor: | M. Ledermann, Jürg Reichen, Abraham Koshy, Sidney Shaw, H. Saegesser, Andrea De Gottardi, Arthur Zimmermann |
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| Rok vydání: | 2005 |
| Předmět: |
Liver Cirrhosis
medicine.medical_specialty Nitric Oxide Synthase Type III Nitric oxide Mice chemistry.chemical_compound Fibrosis Internal medicine Hypertension Portal medicine Animals RNA Messenger Ligation Mice Knockout Endothelin-1 Hepatology business.industry Bile duct medicine.disease Endothelin 1 Mice Inbred C57BL Disease Models Animal Endocrinology medicine.anatomical_structure Liver chemistry Heme Oxygenase (Decyclizing) Hyperdynamic circulation Portal hypertension Bile Ducts Liver function business Heme Oxygenase-1 |
| Zdroj: | Liver International. 25:1044-1052 |
| ISSN: | 1600-0676 1478-3223 |
| Popis: | BACKGROUND/AIMS: It is postulated that nitric oxide (NO) is responsible for the hyperdynamic circulation of portal hypertension. Therefore, we investigated induction of fibrosis and hyperdynamic circulation in endothelial NO synthase knock-out (KO) mice. METHODS: Fibrosis was induced by bile duct ligation. Hemodynamic studies were performed after portal vein ligation. All studies were performed in wild-type (WT) and KO mice. RESULTS: Three to 4 weeks after bile duct ligation (BDL), both WT and KO groups had similar degrees of portal hypertension, 12 (9-14) and 11(8-15) mmHg, median (range), and liver function. Fibrosis increased from 0.0% in sham operated to 1.0 and 1.1% in WT and KO mice, respectively. Cardiac output was similar after portal vein ligation (20 and 17 ml/min in WT and KO mice, respectively). There was no difference in liver of mRNA for endothelin 1, inducible NO synthase (iNOS) and hem-oxygenase 1 (HO1); proteins of iNOS, HO1 and HO2; nor in endothelin A and B (EtA and EtB) receptor density between WT and KO mice after BDL. CONCLUSIONS: These results suggest that endothelial NO synthase is neither essential for the development of fibrosis and portal hypertension in bile duct ligated mice, nor for the hyperdynamic circulation associated with portal hypertension in the portal vein ligated mice. |
| Databáze: | OpenAIRE |
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