Effects of amiloride on the mechanical, electrical and biochemical aspects of ischemia-reperfusion injury

Ken ichi Yano, Toru Maruyama, Naoki Makino, Hirosuke Matsui, Takashi Yanaga

    Research output: Contribution to journalArticlepeer-review

    17 Citations (Scopus)


    Although many causal factors have been proposed for the ischemia-reperfusion injury, the exact mechanisms for interdependent derangements of mechanical, electrical and metabolic events remains unclear. For this purpose, the Langendorff-perfused rat hearts were subjected to regional brief ischemia followed by reperfusion to study the protective effects of amiloride, an inhibitor of Na+-H+ exchange. Amiloride (0.1 mM) attenuated the rise in tissue Na+ and Ca2+, both duration and incidence of arrhythmias (p<0.05 vs. control), sarcolemmal injury (assessed by Na-K ATPase) and lipid peroxidation (assessed by malonedialdehyde formation) during reperfusion. Treatment of hearts with monensin, a sodium inophore, reversed the protective effects of amiloride. Reduction in transsarcolemmal Na+ and pH gradients during ischemia exhibited protective effects similar to those seen with amiloride. These results suggest that cardiac dysfunction, sarcolemmal injury and triggered arrhythmias during ischemia-reperfusion are due to the occurrence of intracellular Ca2+ overload caused by the activation of Na+-H+ exchange and Na+-Ca2+ exchange systems in the myocardium.

    Original languageEnglish
    Pages (from-to)75-83
    Number of pages9
    JournalMolecular and cellular biochemistry
    Issue number1
    Publication statusPublished - Apr 1993

    All Science Journal Classification (ASJC) codes

    • Molecular Biology
    • Clinical Biochemistry
    • Cell Biology


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