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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001613,
umls-concept:C0007776,
umls-concept:C0022655,
umls-concept:C0024485,
umls-concept:C0178719,
umls-concept:C0205082,
umls-concept:C0205173,
umls-concept:C0205421,
umls-concept:C0228174,
umls-concept:C0242184,
umls-concept:C0442805,
umls-concept:C0444706,
umls-concept:C0597484,
umls-concept:C1519355
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pubmed:issue |
2
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pubmed:dateCreated |
1993-4-22
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pubmed:abstractText |
We have used double quantum filtered (DQF) 23Na+ nuclear magnetic resonance (NMR) spectroscopy without shift reagents in order to monitor intracellular Na+ (Na+i) in a cortical brain slice preparation. The external Na+ (Na+o) signal was reduced by 95% by the DQF sequence compared with the directly observed 23Na+. The DQF 23Na+ signal is not exclusively due to Na+i, however, as 40% of this signal appears to arise from Na(+)-ions interacting with extracellular membrane proteins or proteins exposed at the cut surfaces of the slices. Veratridine increased instantly the DQF 23Na+ signal so that it reached 130.4 +/- 5.0% by 12 min. This shows that there was a significant contribution from Na+i in the DQF 23Na+ NMR spectra. Hypoxia of 30 min duration in the presence of 10 nM glucose did not influence intensity of the DQF 23Na+ signal. Aglycaemic hypoxia caused complete collapse of phosphocreatine (PCr) within 7 min whereas DQF 23Na+ first increased 15 min after the insult. This increase reached its maximal value of 125% after 25 min. There was an incomplete recovery of the DQF 23Na+ after aglycaemic hypoxia to 110% of the control value parallel to poor metabolic recovery. The presence of 10 mM extracellular Mg2+ had no apparent effect on the aglycaemic hypoxia-induced rise in Na+i indicating that it was linked to Ca2+ influx. Tetrodotoxin (TTx, 4.7 microM) did not influence the rise of Na+i caused by aglycaemic hypoxia. These results indicate that elevation of Na+i is a late consequence of energy failure in the cerebral cortex.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0959-4965
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
139-42
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pubmed:dateRevised |
2009-9-29
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pubmed:meshHeading |
pubmed-meshheading:8453050-Animals,
pubmed-meshheading:8453050-Anoxia,
pubmed-meshheading:8453050-Cerebral Cortex,
pubmed-meshheading:8453050-Kinetics,
pubmed-meshheading:8453050-Magnetic Resonance Spectroscopy,
pubmed-meshheading:8453050-Quantum Theory,
pubmed-meshheading:8453050-Rats,
pubmed-meshheading:8453050-Rats, Wistar,
pubmed-meshheading:8453050-Sodium
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pubmed:year |
1993
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pubmed:articleTitle |
Delayed increase in intracellular Na+ in cerebral cortical slices during severe hypoxia as measured by double quantum filtered 23Na+ NMR.
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pubmed:affiliation |
Department of Biochemistry and Biotechnology, A.I. Virtanen Institute, University of Kuopio, Finland.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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