| pubmed-article:15453986 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C0010592 | lld:lifeskim |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C2832047 | lld:lifeskim |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C0067684 | lld:lifeskim |
| pubmed-article:15453986 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:15453986 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:15453986 | pubmed:dateCreated | 2004-9-29 | lld:pubmed |
| pubmed-article:15453986 | pubmed:abstractText | Pre- and post-injury Cyclosporin A (CsA) administration has shown neuroprotective properties by ameliorating mitochondrial damage. The aim of this study was to assess the effect of CsA upon N-acetylaspartate (NAA) reduction and ATP loss, two sensitive markers of mitochondrial dysfunction and bioenergetic impairment. Adult male Sprague-Dawley rats were exposed to impact acceleration traumatic brain injury (2 m/450 g) and randomized into the following experimental groups: intrathecal CsA/vehicle treated (n = 12), intravenous CsA/vehicle treated (n = 18) and sham (n = 12). Intrathecal treatment consisted of post-injury (30 min) cisternal bolus of CsA or Vehicle (0.15 mL, 10 mg/kg). Intravenous administration consisted of 30 min post-injury continuous 1 hour infusion of either 20 or 35 mg/kg CsA or Vehicle. Quantitative HPLC analysis of whole brain samples was performed 6 h post-injury for levels of NAA and ATP. Following intrathecal delivery CsA demonstrated significant neuroprotection blunting a 30% NAA reduction (p < 0.001) and restoring 26% of the ATP loss (p < 0.005). The 20 mg/kg intravenous dose failed to ameliorate the biochemical damages while the 35 mg/kg dosage showed 36% NAA recovery and 39% ATP restoration (p < 0.001). In conclusion, CsA is capable of restoring ATP and blunting NAA reduction. Intravenous infusion of 35 mg/kg appears to be the optimal therapeutic strategy in this model. These findings contribute to the notion that CsA achieves neuroprotection, preserving mitochondrial function, and provides a rationale for the assessment of CsA in the clinical setting where MR spectroscopy can monitor NAA and ATP in brain-injured patients. | lld:pubmed |
| pubmed-article:15453986 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15453986 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15453986 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15453986 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15453986 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15453986 | pubmed:issn | 0897-7151 | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:MarmarouAntho... | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:LazzarinoGius... | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:TavazziBarbar... | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:AmoriniAngela... | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:VagnozziRober... | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:SignorettiSte... | lld:pubmed |
| pubmed-article:15453986 | pubmed:author | pubmed-author:DunbarJanaJ | lld:pubmed |
| pubmed-article:15453986 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15453986 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:15453986 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15453986 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15453986 | pubmed:pagination | 1154-67 | lld:pubmed |
| pubmed-article:15453986 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:meshHeading | pubmed-meshheading:15453986... | lld:pubmed |
| pubmed-article:15453986 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15453986 | pubmed:articleTitle | The protective effect of cyclosporin A upon N-acetylaspartate and mitochondrial dysfunction following experimental diffuse traumatic brain injury. | lld:pubmed |
| pubmed-article:15453986 | pubmed:affiliation | Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0508, USA. | lld:pubmed |
| pubmed-article:15453986 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15453986 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15453986 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15453986 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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