rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1998-8-28
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pubmed:abstractText |
Prolonged hypothermic circulatory arrest (HCA) causes clinical neurologic injury. This injury involves neuronal apoptosis, or programmed cell death. We have previously demonstrated that HCA causes glutamate excitotoxicity, increased nitric oxide (NO) production, and NO-mediated apoptosis. We hypothesized that monosialoganglioside GM1 inhibits NO synthase. The purpose of this study was to determine whether GM1 inhibits NO production and neuronal apoptosis after HCA.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
|
pubmed:issn |
0039-6060
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
124
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
298-306
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9706152-Animals,
pubmed-meshheading:9706152-Apoptosis,
pubmed-meshheading:9706152-Cardiopulmonary Bypass,
pubmed-meshheading:9706152-Dentate Gyrus,
pubmed-meshheading:9706152-Dogs,
pubmed-meshheading:9706152-G(M1) Ganglioside,
pubmed-meshheading:9706152-Heart Arrest,
pubmed-meshheading:9706152-Hypothermia, Induced,
pubmed-meshheading:9706152-Injections, Intraventricular,
pubmed-meshheading:9706152-Male,
pubmed-meshheading:9706152-Microdialysis,
pubmed-meshheading:9706152-Microscopy, Electron,
pubmed-meshheading:9706152-Neurons,
pubmed-meshheading:9706152-Neuroprotective Agents,
pubmed-meshheading:9706152-Nitric Oxide Synthase,
pubmed-meshheading:9706152-Nitric Oxide Synthase Type I
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pubmed:year |
1998
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pubmed:articleTitle |
Monosialoganglioside GM1 inhibits neurotoxicity after hypothermic circulatory arrest.
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pubmed:affiliation |
Division of Cardiac Surgery, Johns Hopkins Medicine, Baltimore, MD, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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