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.
ASJC Scopus subject areas
- Radiology Nuclear Medicine and imaging