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

Identifieur interne : 000744 ( PubMed/Corpus ); précédent : 000743; suivant : 000745

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

Auteurs : N B Radford ; E E Babcock ; A. Richman ; L. Szczepaniak ; C R Malloy ; A D Sherry

Source :

RBID : pubmed:9771571

English descriptors

Abstract

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.

PubMed: 9771571

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Le document en format XML

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<div type="abstract" xml:lang="en">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.</div>
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