Rubidium-87 magnetic resonance spectroscopy and imaging for analysis of mammalian K+ transport
Rubidium-87 magnetic resonance spectroscopy and imaging for analysis of mammalian K+ transport
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DOI：
10.1002/nbm.892
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发表时间：
2005-04-01
影响因子：
2.9
通讯作者：
Gruwel, MLH
中科院分区：
文献类型：
--
作者：
Kupriyanov, VV;Gruwel, MLH
本文综述了Rb-87 MRS/I研究哺乳动物细胞、器官和体内K+转运的结果。本文简要介绍了K ~+转运系统及其与Rb ~+的相互作用，并证明Rb ~+是最好的K ~+同源体。Rb-87 MR研究主要集中在离体灌注大鼠和猪心脏，在较小程度上对肾脏，骨骼肌，唾液腺和红细胞。该方法已被用于三个目的：单向Rb+吸收和流出和稳态Rb+水平的动力学测量。在心血管研究中，Rb+在不存在转移试剂的情况下使用，利用主要的细胞内Rb+/K+分布（类似于20：1）。Rb+的吸收和流出的药理学分析允许评估各种转运蛋白的总Rb+通量在大鼠心脏的贡献。已证实Na+/K+ ATP酶负责大部分K+内流，因为Rb+摄取是80%哇巴因敏感的并且依赖于细胞内[Na+]。低流量缺血或代谢抑制引起的能量剥夺降低Rb+摄取率。在正常情况下，Rb+外流主要由电压门控性K+通道介导，K+/Na+/2Cl（-）共转运蛋白的贡献很小。细胞内肿胀和渗透性肿胀刺激Rb+外流的激活假定的K+/H+逆向转运蛋白。ATP敏感性K+（K-ATP）通道的活性通过Rb+流出的代谢（2，4-二硝基苯酚，缺血）或药理学（K-ATP开放剂，P-1075）刺激来显示，这被K-ATP阻断剂格列本脲逆转。线粒体K+运输进行了评估，在心脏与皂苷透性心肌细胞和低温conditions.Three-dimensional（3-D）光谱MRI的离体跳动的猪心脏已被用于获得时间序列的Rb+地图的正常和缺血/梗死的心脏，这表明在受损区域的图像强度较低。缺血区Rb+摄取的动力学依赖于局部血流和代谢。肾上腺素能激动剂多巴酚丁胺刺激Rb+摄取在正常地区，并没有影响摄取在缺血地区。可能影响被动Rb+转运的药物（布美他尼、吡那地尔、格列本脲）在正常或缺血区均未改变Rb+摄取。Rb-87-MRI也能够定位缺血和梗死的血液灌注的心脏。Rb-87 MRS/I是研究离体器官和体内K+转运的良好的非侵入性研究工具。版权所有（c）2005约翰威利T儿子，有限公司.
This review summarizes results Rb-87 MRS/I studies of K+ transport in mammalian cells, organs and in vivo. It provides a brief description of K+ transport systems, their interactions with Rb+ and evidence that Rb+ is a best K+ congener. Rb-87 MR studies have focused mostly on isolated perfused rat and pig hearts and to a lesser extent on kidney, skeletal muscle, salivary gland and red blood cells. The method has been used for three purposes: measurements of kinetics of unidirectional Rb+ uptake and efflux and steady-state Rb+ levels. In cardiovascular studies Rb+ has been used in the absence of shift reagent taking advantage of the predominantly intracellular Rb+/K+ distribution (similar to 20:1). Pharmacological analysis of Rb+ uptake and efflux allowed assessment of the contributions of various transporters to the total Rb+ fluxes in rat hearts. It was confirmed that Na+/K+ ATPase is responsible for the majority of K+ influx since Rb+ uptake is 80% ouabain-sensitive and dependent on the intracellular [Na+]. Energy deprivation caused by low-flow ischemia or metabolic inhibition reduced Rb+ uptake rate. Under normal conditions, Rb+ efflux is mediated mainly by voltage-gated K+ channels with a small contribution from the K+/Na+/2Cl(-) cotransporter. Intracellular alkalosis and osmotic swelling stimulated Rb+ efflux by activation of the putative K+/H+ antiporter. Activity of ATP-sensitive K+ (K-ATP) channels was revealed by metabolic (2,4-dinitrophenol, ischemia) or pharmacological (K-ATP opener, P-1075) stimulation of Rb+ efflux, which was reversed by the K-ATP blocker, glibenclamide. Mitochondrial K+ transport was evaluated in hearts with saponin-permeabilized myocytes and under hypothermic conditions.Three-dimensional (3-D) spectroscopic MRI of isolated beating pig hearts has been used to obtain time series of Rb+ maps of normal and ischemic/infarcted hearts, which showed lower image intensity in the damaged area. Kinetics of Rb+ uptake in the ischemic areas depended on both regional flow and metabolism. The adrenergic agonist dobutamine stimulated Rb+ uptake in normal areas and did not affect uptake in ischemic areas. Drugs that may affect passive Rb+ transport (bumetanide, pinacidil, glibenclamide) did not change Rb+ uptake either in the normal or ischemic zones. Rb-87-MRI was also able to localize ischemia and infarction in blood-perfused hearts. Rb-87 MRS/I is an excellent non-invasive research tool for studies of K+ transport in isolated organs and in vivo. Copyright (c) 2005 John Wiley T Sons, Ltd.