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

✍ Scribed by Dr. Nina B. Radford; Evelyn E. Babcock; Angela Richman; Lidia Szczepaniak; Craig R. Malloy; A. Dean Sherry

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 803 KB
• Volume: 40
• Category: Article
• ISSN: 0740-3194
• DOI: 10.1002/mrm.1910400407

✦ Synopsis

Abstract

The hyperfine shift reagent, TmDOTP^5−^, was used to resolve the ^39^K NMR resonances of intra‐ (K~i~^+^) and extracellular (K~e~^+^) potassium in isolated, perfused guinea pig hearts. [K~i~^+^] as measured by ^39^K NMR was 25.9 ± 10.3 mM, compared with 114.4 ± 10.8 mM as measured by atomic absorption spectros‐copy (AAS) using TmD0TP^5‐^ as a marker of extracellular space. Thus, only approximately 23% of intracellular potassium was detected by ^39^K 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 ^39^K NMR, hearts were perfused with a Rb^+^‐enriched, K^+^ ‐depleted buffer for an extended period. This resulted in loss of the entire ^39^K 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 ^39^K 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 ^39^K in perfused guinea pig hearts.