1991
DOI: 10.1159/000129147
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Reoxygenation Injury following Anoxic Perfusion Preferentially Impairs Bile Acid-Independent Bile Flow

Abstract: We perfused isolated rat livers with Krebs-Ringer buffer, with no recirculation. Bile flow virtually stopped during 30 min of anoxia and resumed following reoxygenation to reach a plateau of 44% of the control level. When taurodehydrocholic acid (TDHC, 50 nmol/ min/g liver) was administered during reoxygenation, bile flow increased three-fold (16.1 ± 1.3 to 45.3 ± 6.3 µl/g liver). The increase in bile output with TDHC was 27.8 µl/g liver, which was 89% of the control output. Bile acid output during this period… Show more

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Cited by 6 publications
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“…Ischemia/ reperfusion injury impairs preferentially bile acid-inde pendent bile flow. 51 To characterize postischemic bile formation in more detail, we quantified the biliary excre tion of actively transported GSH 20,21 and GSSG, 18,19 which partially contribute to the bile acid-independent bile secretion in rat liver. 52 The biliary release of total glutathione and GSSG was markedly decreased during the reflow period.…”
Section: Postischemic Bile Flow and Biliary Glutathione Transportmentioning
confidence: 99%
“…Ischemia/ reperfusion injury impairs preferentially bile acid-inde pendent bile flow. 51 To characterize postischemic bile formation in more detail, we quantified the biliary excre tion of actively transported GSH 20,21 and GSSG, 18,19 which partially contribute to the bile acid-independent bile secretion in rat liver. 52 The biliary release of total glutathione and GSSG was markedly decreased during the reflow period.…”
Section: Postischemic Bile Flow and Biliary Glutathione Transportmentioning
confidence: 99%