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您的检索式：作者名="Manfred Bilzer"
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| 1 | Intravenous administration of glutathione protects parenchymal and non-parenchymal liver cells against reperfusion injury following rat liver transplantation显示文摘AIM:To investigate the effects of intravenous administration of the antioxidant glutathione (GSH) on reperfusion injury following liver transplantation.METHODS:Livers of male Lewis rats were transplanted after 24 h of hypothermic preservation in University of Wisconsin solution in a syngeneic setting. During a 2-h reperfusion period either saline (controls,n=8) or GSH (50 or 100μmol/(h·kg),n=5 each) was continuously administered via the jugular vein.RESULTS:Two hours after starting reperfusion plasma ALT increased to 1 457±281U/L (mean±SE) in controls but to only 908_+187 U/L (P<0.05) in animals treated with 100μmol GSH/(h·kg).No protection was conveyed by 50μmol GSH/(h·kg).Cytoprotection was confirmed by morphological findings on electron microscopy:GSH treatment prevented detachment of sinusoidal endothelial cells (SECs) as well as loss of microvilli and mitochondrial swelling of hepatocytes. Accordingly, postischemic bile flow increased 2-fold. Intravital fluorescence microscopy revealed a nearly complete restoration of sinusoidal blood flow and a significant reduction of leukocyte adherence to sinusoids and postsinusoidal venules. Following infusion of 50μmol and 100 μmol GSH/(h·kg),plasma GSH increased to 65±7mol/L and 97±18μmol/L,but to only 20±3mol/L in untreated recipients.Furthermore, plasma glutathione disulfide (GSSG) increased to 7.5±1.0mol/L in animals treated with 100μmol/(h·kg) GSH but infusion of 50μmol GSH/(h·kg) did not raise levels of untreated controls (1.8±0.5mol/L vs 2.2±0.2mol/L).CONCLUSION:Plasma GSH levels above a critical level may act as a “sink” for ROS produced in the hepatic vasculature during reperfusion of liver grafts.Therefore, GSH can be considered a candidate antioxidant for the prevention of reperfusion injury after liver transplantation, in particular since it has a low toxicity in humans. | RolfJ.Schauer SinanKalmuk Alexander L.Gerbes Rosemarie Leiderer Herbert Meissner Friedrich W.Schildberg Konrad Messmer Manfred Bilzer | 2004 | World Journal of Gastroenterology2004，10，6： | 9 |
| 2 | PI 3-kinase pathway is responsible for antiapoptotic effects of atrial natriuretic peptide in rat liver transplantation显示文摘AIM:To investigate the in vivo effect of atrial natriureticpeptide(ANP)and its signaling pathway during ortho-topic rat liver transplantation.METHODS:Rats were infused with NaCl,ANP(5 μg/kg),wortmannin(WM,16 μg/kg),or a combination ofboth for 20 min.Livers were stored in UW solution(4°C)for 24 h,transplanted and reperfused.Apoptosis wasexamined by caspase-3 activity and TUNEL staining.Phosphorylation of Akt and Bad was visualized by West-ern blotting and phospho-Akt-localization by confocalmicroscopy.RESULTS:ANP-pretreatment decreased caspase-3activity and TUNEL-positive cells after cold ischemia,indicating antiapoptotic effects of ANP in vivo.The an-tiapoptotic signaling of ANP was most likely caused byphosphorylation of Akt and Bad,since pretreatment withPI 3-kinase inhibitor WM abrogated the ANP-inducedreduction of caspase-3 activity.Interestingly,analysis ofliver tissue by confocal microscopy showed translocationof phosphorylated Akt to the plasma membrane of hepa-tocytes evoked by ANP.CONCLUSION:ANP activates the PI-3-kinase pathwayin the liver in vivo leading to phosphorylation of Bad, an event triggering antiapoptotic signaling cascade inischemic liver. | Uwe Grutzner Melanie Keller Michael Bach Alexandra K Kiemer Herbert Meissner Manfred Bilzer Stefan Zahler Alexander L Gerbes Angelika M Vollmar | 2006 | World Journal of Gastroenterology2006，12，7： | 3 |
| 3 | MICROCIRCULATORY FAILURE AFTER RAT LIVER TRANSPLANTATION IS RELATED TO KUPFFER CELL-DERIVED OXIDANT STRESS BUT NOT INVOLVED IN EARLY GRAFT DYSFUNCTION1显示文摘 | Rolf J. Schauer Manfred Bilzer Sinan Kalmuk Alexander L. Gerbes Rosmarie Leiderer Friedrich W. Schildberg Konrad Messmer | 2001 | Transplantation2001，，10： | 1 |
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