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  • 1
    Electronic Resource
    Electronic Resource
    DISCUSSION PAPER STUDIES ON SERUM ALKALINE PHOSPHATASE ISOENZYMES (1969)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 166 (1969), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1969.tb54318.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanisms of biliary excretion of lithocholate-3-sulfate in Eisai hyperbilirubinemic rats (EHBR) (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 1792-1797 
    Details
    ISSN: 1573-2568
    Keywords: bile acid ; organic anion ; biliary excretion ; hepatic transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Biliary excretion of lithocholate-3-sulfate is markedly impaired in EHBR. To examine the mechanism of biliary lithocholate-3-sulfate excretion in EHBR, the effects of colchicine treatment, a vesicular transport inhibitor, and infusion of taurocholate and organic anions were studied in EHBR and Sprague-Dawley rats. Colchicine treatment and taurocholate infusion had no effect on biliary lithocholate-3-sulfate excretion in EHBR, suggesting that biliary lithocholate-3-sulfate excretion is not mediated by the vesicular transport or by the bile acid excretory pathway. In control Sprague-Dawley rats, both sulfobromophthalein and dibromosulfophthalein infusion inhibited biliary lithocholate-3-sulfate excretion. In contrast, in EHBR dibromosulfophthalein infusion inhibited biliary lithocholate-3-sulfate excretion but BSP infusion did not. Indocyanine green and pravastatin infusion did not affect biliary lithocholate-3-sulfate excretion but pravastatin infusion had no effect in EHBR. These findings indicate that, whether physiologically important or not, two or more excretory pathways for organic anions exist at the canalicular membrane other than the ATP-dependent one.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02212704
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of ursodeoxycholate and its conjugates on biliary glutathione excretion in rats (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 1953-1958 
    Details
    ISSN: 1573-2568
    Keywords: bile acid ; ursodeoxycholate ; glucuronide ; sulfate ; glutathione ; biliary excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of ursodeoxycholate and its conjugates on biliary glutathione excretion were studied in rats. Ursodeoxycholate had no effect on glutathione excretion, but tauroursode-oxycholate (10µmol/100 g body wt) transitionally increased biliary glutathione excretion. Ursodeoxycholate-3-O-glucuronide (2 and 10µmol/100 g body wt) markedly inhibited biliary glutathione excretion, but ursodeoxycholate-3-sulfate (2µmol/100 g body wt) and ursode-oxycholate-3,7-disulfate (10µmol/100 g body wt) did not. These findings indicate the existence of several biliary excretion pathways for bile acid glucuronides and sulfates and that one of them for the glucuronides is shared by biliary glutathione excretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02093595
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  • 4
    Electronic Resource
    Electronic Resource
    Changes in biliary excretory mechanisms in bile duct-ligated rat (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 256-262 
    Details
    ISSN: 1573-2568
    Keywords: obstructive jaundice ; bile acid ; bile flow ; glutathione ; biliary lipid ; bile duct ligation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of bile duct ligation on biliary excretion of bile acids, glutathione, and lipids were studied in the rat. The bile duct of the rat was ligated for three days. The biliary bile acid excretion after bile duct cannulation was higher at first, but after 90 min became lower than that in the control rat. The bile flow in the bile duct-ligated rat was higher after bile duct cannulation and gradually decreased to the same level as in the control rat. Biliary glutathione excretion, which has been suggested to be a driving force for the bile acid-independent canalicular bile flow, was markedly decreased in the bile duct-ligated rat. The mannitol clearance was increased and the bile ductules showed proliferation in the bile duct-ligated rat, suggesting an increase in the ductular bile flow. Biliary excretion of lithocholate glucuronide was more markedly impaired than that of taurocholate. When taurocholate was infused at higher rates, which increases bile flow and biliary excretion of bile acid and lipids in the control rat, biliary bile acid and lipid excretion remained constant in the bile duct-ligated rat. These findings indicate that, in the bile duct-ligated rat, the ductular bile flow was increased and bile acid-independent canalicular bile flow was decreased and that, although the biliary excretion of bile acids was not as impaired as that of organic anions, the capacity of bile acid and lipid excretion was markedly decreased.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02093813
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  • 5
    Electronic Resource
    Electronic Resource
    Lithocholate-3-O-glucuronide-induced cholestasis (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 1543-1548 
    Details
    ISSN: 1573-2568
    Keywords: cholestasis ; lithocholate-3-O-glucuronide ; tauroursodeoxycholate ; ursodeoxycholate-3-O-glucuronide ; congenital hyperbilirubinemic rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanism of lithocholate-3-O-glucuronide-induced cholestasis is unknown. In this study, we investigated the cholestatic effects of this agent in a congenital hyperbilirubinemic rat, EHBR. We also studied the effects of ursodeoxycholate-3-O-glucuronide and tauroursodeoxycholate on lithocholate-3-O-glucuronide-induced cholestasis in rats. Lithocholate-3-O-glucuronide, administered at the rate of 0.1 μmol/min/100 g for 40 min, a cholestatic dose in control rats, failed to cause cholestasis in EHBR, and biliary lithocholate-3-O-glucuronide excretion was delayed. Biliary concentrations of this agent did not correlate with the severity of cholestasis. Both tauroursodeoxycholate and ursodeoxycholate-3-O-glucuronide, infused at the rate of 0.2 μmol/min/100 g for 120 min, completely inhibited cholestasis induced by lithocholate-3-O-glucuronide administered at the rate of 0.1 μmol/min/100 g for 40 min. Only tauroursodeoxycholate enhanced biliary lithocholate-3-O-glucuronide excretion. These findings indicate that lithocholate-3-O-glucuronide-induced cholestasis is induced by damage at the level of the bile canalicular membrane. Ursodeoxycholate-3-O-glucuronide inhibits this cholestasis, possibly by inhibiting the access of lithocholate-3-O-glucuronide to the bile canalicular membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01308618
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  • 6
    Electronic Resource
    Electronic Resource
    Enhanced Biliary Excretion of Lithocholate-3-Sulfate by Ursodeoxycholate-3,7-disulfate Infusion in Eisai Hyperbilirubinemic Rat (EHBR) (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 188-192 
    Details
    ISSN: 1573-2568
    Keywords: LITHOCHOLATE-3-SULFATE ; URSODEOXYCHOLATE-3,7-DISULFATE ; BILE ACIDS ; BILIARY EXCRETION ; EISAI HYPERBILIRUBINEMIC RATS (EHBR) ; PROTEIN BINDING
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Biliary excretion of lithocholate-3-sulfate andursodeoxycholate 3,7-disulfate is markedly impaired inEHBR. In the present study, the effects ofursodeoxycholate 3,7-disulfate infusion onlithocholate-3-sulfate excretion were studied in EHBR andSprague-Dawley rats. Although in control rats,ursodeoxycholate 3,7-disulfate infusion had no effect onbiliary lithocholate-3-sulfate excretion, in EHBR itenhanced biliary lithocholate-3-sulfate excretion. Althoughursodeoxycholate 3,7-disulfate dose-dependentlyinhibited lithocholate-3-sulfate binding by rat serumalbumin and rat liver cytosol, it did not affect theserum clearance of lithocholate-3-sulfate in EHBR invivo. These findings indicate that in EHBR, in which themajor ATP-dependent organic anion transporter isimpaired, the excretory pathway for ursodeoxycholate 3,7-disulfate may interact to that forlithocholate-3-sulfate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018809028425
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  • 7
    Electronic Resource
    Electronic Resource
    Epstein-Barr virus infection resembling autoimmune hepatitis with lactate dehydrogenase and alkaline phosphatase anomaly (1999)
    Springer
    Journal of gastroenterology 34 (1999), S. 706-712 
    Details
    ISSN: 1435-5922
    Keywords: Key words: Epstein-Barr virus infection ; autoimmune hepatitis ; autoimmunization ; lactate dehydrogenase anomaly ; alkaline phosphatase anomaly
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: A 73-year-old man had fever, lymphadenopathy, granulocytopenia, thrombocytopenia, ascites, pleural effusion, liver injury, and an allergic-like skin rash. Autoantibodies, such as anti-nuclear antibody, were shown, and there were lactate dehydrogenase and alkaline phosphatase anomalies and platelet-associated IgG. His liver injury resembled that in autoimmune hepatitis. He was diagnosed with Epstein-Barr virus (EBV) infection associated with autoimmunization because of his clinical course, fluctuation of anti EBV antibodies and positive EBV genome in circulating lymphocytes and serum. This case suggests a close relationship between EBV infection and autoimmunization or autoimmune-like hepatitis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005350050324
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  • 8
    Electronic Resource
    Electronic Resource
    Guide for judicious use of the paracetamol absorption technique in a study of gastric emptying rate of liquids (1998)
    Springer
    Journal of gastroenterology 33 (1998), S. 785-791 
    Details
    ISSN: 1435-5922
    Keywords: Key words: gastric emptying rate ; paracetamol (acetaminophen) ; pharmacokinetics ; rate of absorption
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: The paracetamol absorption technique, a widely used method for evaluating the gastric emptying rate of liquids, appears to be performed inappropriately, resulting from a lack of consideration of pharmacokinetics in paracetamol absorption. This review suggests that appropriate study designs and logical choice of the parameters for the rate of paracetamol absorption are the cornerstone of reliable investigation of gastric emptying using the paracetamol method.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005350050177
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of Organic Anions and Bile Acid Conjugates on Biliary Excretion of Pravastatin in the Rat (1998)
    Springer
    Pharmaceutical research 15 (1998), S. 72-76 
    Details
    ISSN: 1573-904X
    Keywords: organic anions ; bile acids ; pravastatin ; canalicular multispecific organic anion transporter (cMOAT) ; Eisai hyperbilirubinemic rats (EHBR)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. Biliary organic anion excretion is mediated by an ATP-dependent primary active transporter, a so-called canalicular multispecific organic anion transporter (cMOAT). As there appear to be many canalicular organic anion transports, we examined the effects of various organic anions and bile acid conjugates on the biliary excretion of pravastatin in rats. Methods. [l4C]pravastatin was intravenously injected into rats with bile drainage in the presence and absence of the continuous infusion of organic anions and bile acids, and radioactivity of its biliary excretion was studied. Results. Biliary excretion of [14C]pravastatin was markedly inhibited by sulfobromophthalein-glutathione, taurolithocholate-3-sulfate, ursodeoxycholate-3,7-sulfate, and ursodeoxycholate-3-O-glucuronide. In contrast, dibromosulfophthalein only slightly inhibited biliary pravastatin excretion, and cefpiramide did not affect biliary pravastatin excretion. Conclusions. These findings further support the multiplicity of canalicular organic anion transport, and pravastatin is considered to be excreted through a canalicular transporter which is absent in EHBR in addition to through cMOAT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1011900820409
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