부산대학교 도서관

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 µMacetoxymethyl ester of the indicator. Basal Mgiconcentrations measured by three different indicators averaged 0.85 ± 0.10 mM(n= 9) and showed no correlation with the KDof 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 Mgiduring loading with fluorinated o-aminophenol-N,N,O-triacetate. Between 10 and 15 min of ischemia, Mgirose nearly 3-fold to 2.1 ± 0.4 mM. This increase in Mgioccurred over the same time course as the decrease in ATP. After 20 min of reperfusion with Krebs-Henseleit buffer, Mgideclined to 1.5 ± 0.5 mM. This sustained elevation of Mgiabove 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.