Effects of L-glutamine on post-ischaemic cardiac function: Protection and rescue

Shihab E. O. Khogali, Alexander A. Harper, Jenni A. Lyall, Michael J. Rennie (Lead / Corresponding author)

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    68 Citations (Scopus)

    Abstract

    We investigated the effects of L-glutamine (0-20 mM) on cardiac function. The isolated perfused working rat heart (left atrial and aortic pressures of 5 and 70 cm H2O, respectively) was subjected to 20 min of normothermic low-flow ischaemia followed by reperfusion for 35 min. In the absence of glutamine, ischaemia-reperfusion caused an immediate significant (P < 0.01) fall in cardiac output from 46 to 20 ml/min, with a further deterioration to 17 ml/min at 35 min reperfusion. Ischaemia also caused a significant (P < 0.05) fall in myocardial glutamate from 2.6 to 1.8 μmol/g wet weight: and ischaemia-reperfusion caused significant (each P < 0.05) diminutions of myocardial ATP from 3.5 to 1.0 μmol/g wet weight and phosphocreatine from 4.8 to 1.5 μmol/g wet weight and resulted in significant (P < 0.05) accumulation of myocardial lactate from 0.9 to 4.3 μmol/g wet weight. Glutamine, present throughout the perfusion protocol (i.e. prior to ischaemia), at or above 1.25 mM, prevented the post-ischaemic diminution of cardiac output and the deleterious changes in myocardial metabolites. Post-ischaemic treatment with glutamine at 2.5 mM completely prevented the post-ischaemic diminution of cardiac output and restored the myocardial metabolites to normal. Conclusions: glutamine may be suitable as a cardioprotective and rescue agent. These effects may be mediated by maintenance of myocardial glutamate, ATP and phosphocreatine; and prevention of lactate accumulation.

    Original languageEnglish
    Pages (from-to)819-827
    Number of pages9
    JournalJournal of Molecular and Cellular Cardiology
    Volume30
    Issue number4
    DOIs
    Publication statusPublished - Apr 1998

    Keywords

    • ATP
    • Glutamate
    • Glutamine
    • Lactate
    • Myocardial ischaemia
    • Phosphocreatine

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