Radford N B, Babcock E E, Richman A, Szczepaniak L, Malloy C R, Sherry A D
University of Texas Southwestern Medical Center, Dallas, USA.
Magn Reson Med. 1998 Oct;40(4):544-50. doi: 10.1002/mrm.1910400407.
The hyperfine shift reagent, TmDOTP5-, was used to resolve the 39K NMR resonances of intra- (Ki+) and extracellular (Ke+) potassium in isolated, perfused guinea pig hearts. [Ki+] 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 TmDOTP5- 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 Ki+ signal increased during early ischemia then returned to baseline levels during reperfusion. In an effort to learn more about the Ki+ 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 Ki+, as measured by AAS, decreased from approximately 60 to approximately 6 to 7 micromol/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 Ki+ 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.
