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缺血大鼠心脏中的胞质游离镁水平。

Cytosolic free magnesium levels in ischemic rat heart.

作者信息

Murphy E, Steenbergen C, Levy L A, Raju B, London R E

机构信息

Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.

出版信息

J Biol Chem. 1989 Apr 5;264(10):5622-7.

PMID:2925624
Abstract

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.

摘要

在灌注的大鼠心脏中,通过19F NMR测量心肌缺血期间胞质游离镁离子浓度(Mgi)的变化,该心脏预先加载了镁螯合剂邻氨基酚 - N,N,O - 三乙酸的氟标记衍生物。通过用含有5 microM指示剂乙酰氧基甲酯的200 - 400 ml Krebs - Henseleit缓冲液灌注,将适当的镁指示剂细胞内加载到灌注的大鼠心脏中。用三种不同指示剂测量的基础Mgi浓度平均为0.85±0.10 mM(n = 9),并且与所用指示剂的KD没有相关性。通过31P NMR测量ATPα - 和β - 磷酸之间的镁依赖性位移表明,在用氟化邻氨基酚 - N,N,O - 三乙酸加载期间,Mgi没有可测量的降低。在缺血10至15分钟之间,Mgi上升近3倍至2.1±0.4 mM。Mgi的这种增加与ATP的减少发生在相同的时间进程中。在用Krebs - Henseleit缓冲液再灌注20分钟后,Mgi下降至1.5±0.5 mM。Mgi持续高于基础水平的升高可能会抑制肌浆网中钙的释放,从而导致在可逆性缺血期后发生的机械功能损害,这一点已有充分记录。

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