Reoxygenation injury following anoxic perfusion preferentially impairs bile acid-independent bile flow.

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 microliters/g liver). The increase in bile output with TDHC was 27.8 microliters/g liver, which was 89% of the control output. Bile acid output during this period was 1.4 mumol/g liver, which was 93% of the control level. Addition of allopurinol (50 nmol/min/g liver) without TDHC increased bile flow significantly (16.1 +/- 1.3 to 21.3 +/- 1.2 microliters/g liver), but the change was not significant when allopurinol and TDHC were given. The addition of allopurinol also reduced the cumulative release of lactate dehydrogenase from the liver during the reoxygenation period, but had no effect on hepatic adenosine triphosphate levels. Our data suggest that the bile acid-independent bile flow is sensitive to reoxygenation injury following anoxia whereas bile acid output and bile acid-dependent bile flow are resistant.