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

The hyperfine shift reagent, TmDOTP^5-, 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.