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Evaluation of myoca'Rdial viability and eneRgetics Regulated by intracellulae free Mg^<2+>.

心肌活力和由细胞内游离Mg 2 调节的能量的评价。

基本信息

批准号：
07671487
负责人：
MASUDA Takashi
金额：
$ 1.54万
依托单位：
KITASATO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1997
项目状态：
已结题

项目摘要

The aim of this study was to measure the concentration of intracellular free magnesium (free [Mg<@D12+@>D1] i) in isolated rat heart by analyzing<@D131@>D1P NMR spectra obtained from the linear prediction z-transform method (LPZAR), and to investigate the effect of extracellular inorganic phosphate ([Pi] o) on myocardial Mg metabolism. Free [Mg<@D12+@>D1] i of Langendorff perfused hearts was assessed by <@D131@>D1P NMR spectroscopy using LPZAR.The ionic enviroment was altered by changing [Pi] o from 1.2 to 5.0 mM in Krebs-Henseleit buffer during heart perfusion (n=6). Chenges in free [Mg<@D12+@>D1] i were calculated from the frequency difference between alpha-and beta-ATP in the<@D131@>D1P NMR spectrum. The spectra obtained using LPZAR provided peaks sharp enough for the calculation of free [Mg S12+ E1] i and distinct chemical shift of beta-peak of ATP enabled to estimate the change of free [Mg<@D12+@>D1] i. Wten [Pi] o was increased from 1.2 mM of normal concentration to 5.0 mM and then restored to 1.2 mM,free [Mg S12+ E1] i decreased significantly from 0.525(]SY.+-。[)0.048 mM to 0.407(]SY.+-。[)0.025 mM and returned to the control level of 0.601(]SY.+-。[)0.053 mM.The net movement of free Mg<@D12+@>D1 may involve Mg<@D12+@>D1-Pi exchange mechanism across the plasma membrane in rat heart, as the increase in extracellular [Pi] resulted in the decrease in free [Mg<@D12+@>D1] i.

本研究的目的是通过分析线性预测z变换法(LPZAR)获得的~lt；@D131@&gt；D1P核磁共振波谱，测定大鼠离体心细胞内游离镁([mg&lt；@D12+@&gt；d1]i)的浓度，并探讨细胞外无机磷([PI]o)对心肌镁代谢的影响。用~lt；@D131@&gt；D1P核磁共振波谱用LPZAR测定Langendorff灌流心脏的游离[mg&lt；@D12+@&gt；d1]i。在心脏灌流过程中，通过改变Krebs-Henseleit缓冲液中的[Pi]o从1.2 mM到5.0 mM来改变离子环境(n=6)。[mg&lt；@d12+@&gt；d1]i的成熟度是根据&lt；@d131@&gt；d1P核磁共振谱中α-和β-三磷酸腺苷的频率差计算出来的。利用LPZAR获得的光谱提供了足够锐利的峰来计算游离[mg S12+E_1]i，并且三磷酸腺苷的β-峰明显的化学位移使得能够估计游离[mg&lt；@D12+@&gt；D_1]i的变化。WTEN[PI]o从正常浓度的1.2mM增加到5.0mM，然后恢复到1.2mM，游离的[mg S12+E_1]i从0.525(]sy.+-显著下降。[)0.048 mm至0.407(]正负。[)0.025 mm，并返回到0.601(]sy+-的控制水平。[)0.053 mM。细胞外[PI]升高导致游离[mg&lt；@d12+@&gt；d1]i减少，可能与心肌细胞内游离[mg12+@gt；d1]d1跨质膜的镁磷交换机制有关。