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.