title: Sodium TQF NMR and intracellular sodium in isolated crystalloid perfused rat heart.
abstract: The feasibility of monitoring intracellular sodium changes using Na triple quantum filtered NMR without a chemical shift reagent (SR) was investigated in an isolated rat heart during a variety of interventions for Na(i) loading. Perfusion with 1 mM ouabain or without K+ present in the perfusate for 30 min produced a rise of the Na TQF signal with a plateau of approximately 190% and approximately 228% relative to the preintervention level, respectively. Stop-flow ischemia for 30 min resulted in a TQF signal growth of approximately 147%. The maximal Na TQF signal increase of 460% was achieved by perfusion without K+/Ca2+, corresponding to an elimination of the Na transmembrane gradient. The observed values of Na NMR TQF growth in the physiological and pathological ranges are in agreement with reported data by other methods and have a linear correlation with intracellular sodium content as determined in this study by Co-EDTA method and by sucrose-histidine washout of the extracellular space. Our data indicate that the increase in Na TQF NMR signal is determined by the growth of Na(i), and the extracellular Na contribution to the total TQF signal is unchanged at approximately 64%. In conclusion, Na TQF NMR without using SR offers a unique and noninvasive opportunity to monitor alterations of intracellular sodium. It may provide valuable insights for developing cardioprotective strategies and for observing the effects of pharmaceutical treatments on sodium homeostasis.
authors.affiliation: Center for Functional Imaging, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.
authors.forename: V D
authors.initials: VD
authors.lastname: Schepkin
authors.forename: I O
authors.initials: IO
authors.lastname: Choy
authors.forename: T F
authors.initials: TF
authors.lastname: Budinger
authors.forename: D Y
authors.initials: DY
authors.lastname: Obayashi
authors.forename: S E
authors.initials: SE
authors.lastname: Taylor
authors.forename: W M
authors.initials: WM
authors.lastname: DeCampli
authors.forename: S C
authors.initials: SC
authors.lastname: Amartur
authors.forename: J N
authors.initials: JN
authors.lastname: Young
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002614:Chelating Agents; D004492:Edetic Acid; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D006321:Heart / Q000187:drug effects; D006639:Histidine / Q000494:pharmacology; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D010477:Perfusion; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism*; D013395:Sucrose / Q000494:pharmacology
chemical_list: D002614:Chelating Agents; D004791:Enzyme Inhibitors; D006639:Histidine; D013395:Sucrose; D010042:Ouabain; D004492:Edetic Acid; D012964:Sodium; D008274:Magnesium; D011188:Potassium; D002118:Calcium