Does myocardial ischemia increase cytosolic free magnesium levels in perfused rat hearts?
Myocardial ischemia causes a significant, sustained increase in cytosolic free magnesium that persists during reperfusion, potentially contributing to post-ischemic mechanical dysfunction.
Changes in cytosolic free magnesium ion concentration (Mgi) during myocardial ischemia were measured by 19F NMR in perfused rat hearts loaded with fluorine-labeled derivatives of the magnesium chelator o-aminophenol-N,N,O-triacetate. The perfused rat hearts were loaded intracellularly with the appropriate magnesium indicator by perfusion with 200-400 ml of Krebs-Henseleit buffer containing 5 microM acetoxymethyl ester of the indicator. Basal Mgi concentrations measured by three different indicators averaged 0.85 +/- 0.10 mM (n = 9) and showed no correlation with the KD of the indicator used. 31P NMR measurements of the magnesium-dependent shift between alpha- and beta-phosphates of ATP demonstrate that there is no measurable lowering of Mgi during loading with fluorinated o-aminophenol-N,N,O-triacetate. Between 10 and 15 min of ischemia, Mgi rose nearly 3-fold to 2.1 +/- 0.4 mM. This increase in Mgi occurred over the same time course as the decrease in ATP. After 20 min of reperfusion with Krebs-Henseleit buffer, Mgi declined to 1.5 +/- 0.5 mM. This sustained elevation of Mgi above basal levels may inhibit calcium release from sarcoplasmic reticulum, thereby contributing to the well documented impairment of mechanical function that occurs after a reversible period of ischemia.
Murphy et al. (Sat,) studied this question.
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