39K NMR measurement of intracellular potassium during ischemia in the perfused guinea pig heart

Nina B. Radford, Evelyn E. Babcock, Angela Richman, Lidia Szczepaniak, Craig R. Malloy, A. Dean Sherry

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


The hyperfine shift reagent, TmDOTP5-, was used to resolve the 39K NMR resonances of intra- (K(i)+) and extracellular (K(e)+) potassium in isolated, perfused guinea pig hearts. [K(i)+] as measured by 39K NMR was 25.9 ± 10.3 mM, compared with 114.4 ± 10.8 mM as measured by atomic absorption spectroscopy (AAS) using TmDOTP-5 as a marker of extracellular space. Thus, only approximately 23% of intracellular potassium was detected by 39K NMR using our experimental conditions. The area of the K(i)+ signal increased during early ischemia then returned to baseline levels during reperfusion. In an effort to learn more about the K(i)+ not detected by 39K NMR, hearts were perfused with a Rb+-enriched, K+-depleted buffer for an extended period. This resulted in loss of the entire 39K NMR signal, and K(i)+, as measured by AAS, decreased from ~60 to ~6 to 7 μmol/g wet weight. When K+-depleted hearts were subjected to global ischemia, a small 39K NMR signal reappeared, suggesting that at least a portion of the nonexchangeable K(i)+ becomes detectable by NMR during ischemia. This newly visible K+ signal subsequently dissipated during reperfusion of ischemic hearts. We conclude that ischemia induces changes in the NMR visibility of 39K in perfused guinea pig hearts.

Original languageEnglish (US)
Pages (from-to)544-550
Number of pages7
JournalMagnetic resonance in medicine
Issue number4
StatePublished - Oct 1998


  • Cations
  • Ischemia
  • NMR
  • Potassium

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging


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