Decrease of ischemic injury to the isolated perfused rat liver by loop diuretics

Hepatology : Official Journal of the American Association for the Study of Liver Diseases
R J FiegenH de Groot

Abstract

Recent studies suggest a major role played by sodium in the pathogenesis of ischemic liver injury: in these studies, sodium-free media have been shown to offer protection against hypoxic injury to isolated hepatocytes. As sodium-free perfusions of the isolated rat liver proved impossible because of extensive vasoconstriction, we assessed the effects of two inhibitors of the Na+-K+-2Cl- cotransporter, the loop diuretics furosemide and bumetanide, on ischemic liver injury. In untreated control livers lactate dehydrogenase (LDH) efflux immediately after reperfusion after 60 minutes of ischemia at 37 degrees C was 1666 +/- 473 U/L. When livers were pretreated with furosemide or bumetanide before the ischemic period, LDH efflux was only 773 +/- 292 U/L and 702 +/- 183 U/L respectively (P < .01). LDH activity in the effluent of the pretreated livers remained significantly below the values of ischemic control livers for the whole reperfusion period of 90 minutes. Bile flow in the postischemic phase was improved by pretreatment with furosemide or bumetanide. The increase in intracellular sodium, as measured by 23Na-NMR, was attenuated from 193% +/- 71% during 60 minutes of ischemia in controls to 148% +/- 80% after bumetanide applicati...Continue Reading

Citations

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