39K NMR measurement of intracellular potassium during ischemia in the perfused guinea pig heart.
Identifieur interne : 000728 ( PubMed/Checkpoint ); précédent : 000727; suivant : 00072939K NMR measurement of intracellular potassium during ischemia in the perfused guinea pig heart.
Auteurs : N B Radford [États-Unis] ; E E Babcock ; A. Richman ; L. Szczepaniak ; C R Malloy ; A D SherrySource :
- Magnetic resonance in medicine [ 0740-3194 ] ; 1998.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Potassium.
- chemical : Organometallic Compounds, Organophosphorus Compounds, Thulium.
- metabolism : Myocardial Ischemia, Myocardium.
- methods : Magnetic Resonance Spectroscopy.
- Animals, Guinea Pigs, Perfusion, Spectrophotometry, Atomic.
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
Affiliations:
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pubmed:9771571Le document en format XML
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<term>Myocardium (metabolism)</term>
<term>Organometallic Compounds</term>
<term>Organophosphorus Compounds</term>
<term>Perfusion</term>
<term>Potassium (metabolism)</term>
<term>Spectrophotometry, Atomic</term>
<term>Thulium</term>
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<term>Cochons d'Inde</term>
<term>Composés organiques du phosphore</term>
<term>Composés organométalliques</term>
<term>Ischémie myocardique (métabolisme)</term>
<term>Myocarde (métabolisme)</term>
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<term>Spectrophotométrie atomique</term>
<term>Spectroscopie par résonance magnétique ()</term>
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<front><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>
</front>
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<Abstract><AbstractText>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.</AbstractText>
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