| pubmed-article:10027772 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C0010097 | lld:lifeskim |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C0162512 | lld:lifeskim |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C1882598 | lld:lifeskim |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C0007786 | lld:lifeskim |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C0067684 | lld:lifeskim |
| pubmed-article:10027772 | lifeskim:mentions | umls-concept:C1704711 | lld:lifeskim |
| pubmed-article:10027772 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10027772 | pubmed:dateCreated | 1999-3-18 | lld:pubmed |
| pubmed-article:10027772 | pubmed:abstractText | Brain N-acetylaspartate (NAA) can be quantified by in vivo proton magnetic resonance spectroscopy (1H-MRS) and is used in clinical settings as a marker of neuronal density. It is, however, uncertain whether the change in brain NAA content in acute stroke is reliably measured by 1H-MRS and how NAA is distributed within the ischemic area. Rats were exposed to middle cerebral artery occlusion. Preischemic values of [NAA] in striatum were 11 mmol/L by 1H-MRS and 8 mmol/kg by HPLC. The methods showed a comparable reduction during the 8 hours of ischemia. The interstitial level of [NAA] ([NAA]e) was determined by microdialysis using [3H]NAA to assess in vivo recovery. After induction of ischemia, [NAA]e increased linearly from 70 micromol/L to a peak level of 2 mmol/L after 2 to 3 hours before declining to 0.7 mmol/L at 7 hours. For comparison, [NAA]e was measured in striatum during global ischemia, revealing that [NAA]e increased linearly to 4 mmol/L after 3 hours and this level was maintained for the next 4 h. From the change in in vivo recovery of the interstitial space volume marker [14C]mannitol, the relative amount of NAA distributed in the interstitial space was calculated to be 0.2% of the total brain NAA during normal conditions and only 2 to 6% during ischemia. It was concluded that the majority of brain NAA is intracellularly located during ischemia despite large increases of interstitial [NAA]. Thus, MR quantification of NAA during acute ischemia reflects primarily changes in intracellular levels of NAA. | lld:pubmed |
| pubmed-article:10027772 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10027772 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10027772 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10027772 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10027772 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10027772 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10027772 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10027772 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:10027772 | pubmed:issn | 0271-678X | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:HansenA JAJ | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:SandsJ AJA | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:LaursenHH | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:Fink-JensenAA | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:RosenbaumSS | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:ToppSS | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:StensgaardAA | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:HedehusMM | lld:pubmed |
| pubmed-article:10027772 | pubmed:author | pubmed-author:ValsborgJ SJS | lld:pubmed |
| pubmed-article:10027772 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10027772 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:10027772 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10027772 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10027772 | pubmed:pagination | 164-72 | lld:pubmed |
| pubmed-article:10027772 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
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| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
| pubmed-article:10027772 | pubmed:meshHeading | pubmed-meshheading:10027772... | lld:pubmed |
| pubmed-article:10027772 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10027772 | pubmed:articleTitle | N-Acetylaspartate distribution in rat brain striatum during acute brain ischemia. | lld:pubmed |
| pubmed-article:10027772 | pubmed:affiliation | Department of Neuroendocrinology, Novo Nordisk A/S, Maaloer, Denmark. | lld:pubmed |
| pubmed-article:10027772 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10027772 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10027772 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10027772 | lld:pubmed |
