Changes in cytosolic free magnesium ion concentration (Mg(i)) 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 μM acetoxymethyl ester of the indicator. Basel Mg(i) concentrations measured by three different indicators averaged 0.85 ± 0.10 mM (n = 9) and showed no correlation with the K(D) of the indicator used. 31P NMR measurements of the magnesium-dependent shift between α- and β-phosphates of ATP demonstrate that there is no measurable lowering of Mg(i) during loading with fluorinated o-aminophenol-N,N,O-triacetate. Between 10 and 15 min of ischemia. Mg(i) rose nearly 3-fold to 2.1 ± 0.4 mM. This increase in Mg(i) occurred over the same time course as the decrease ATP. After 20 min of reperfusion with Krebs-Henseleit buffer, Mg(i) declined to 1.5 ± 0.5 mM. This sustained elevation of Mg(i) 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.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Biological Chemistry|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology