| pubmed-article:8453050 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0007776 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0022655 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0001613 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0228174 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0205082 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0444706 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0024485 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0205173 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C0205421 | lld:lifeskim |
| pubmed-article:8453050 | lifeskim:mentions | umls-concept:C1519355 | lld:lifeskim |
| pubmed-article:8453050 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8453050 | pubmed:dateCreated | 1993-4-22 | lld:pubmed |
| pubmed-article:8453050 | 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. | lld:pubmed |
| pubmed-article:8453050 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8453050 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8453050 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8453050 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8453050 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8453050 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8453050 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8453050 | pubmed:issn | 0959-4965 | lld:pubmed |
| pubmed-article:8453050 | pubmed:author | pubmed-author:BrooksK JKJ | lld:pubmed |
| pubmed-article:8453050 | pubmed:author | pubmed-author:KauppinenR... | lld:pubmed |
| pubmed-article:8453050 | pubmed:author | pubmed-author:PirttiläT RTR | lld:pubmed |
| pubmed-article:8453050 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8453050 | pubmed:volume | 4 | lld:pubmed |
| pubmed-article:8453050 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8453050 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8453050 | pubmed:pagination | 139-42 | lld:pubmed |
| pubmed-article:8453050 | pubmed:dateRevised | 2009-9-29 | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:meshHeading | pubmed-meshheading:8453050-... | lld:pubmed |
| pubmed-article:8453050 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8453050 | pubmed:articleTitle | Delayed increase in intracellular Na+ in cerebral cortical slices during severe hypoxia as measured by double quantum filtered 23Na+ NMR. | lld:pubmed |
| pubmed-article:8453050 | pubmed:affiliation | Department of Biochemistry and Biotechnology, A.I. Virtanen Institute, University of Kuopio, Finland. | lld:pubmed |
| pubmed-article:8453050 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8453050 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:8453050 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
