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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1998-8-4
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pubmed:abstractText |
Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 h of HCA at 18 degrees C, and rewarmed to 37 degrees C on closed-chest cardiopulmonary bypass. All animals were mechanically ventilated and monitored for 20 h before extubation and survived for 3 days. Group 1 dogs (n = 6) were pretreated with GM1, 30 mg/kg/24 h for 3 days before HCA, and received continuous infusion of GM1 during the procedure and 30 mg/kg/24 h for 3 days after HCA. Group 2 dogs (n = 6) received vehicle only. With a species-specific behavior scale that yielded a neurodeficit score ranging from 0% (normal) to 100% (brain dead), all animals were neurologically assessed every 12 h by two observers. After death at 72 h, brains were examined by glutamate receptor autoradiography and by histologic examination for patterns of selective neuronal necrosis and were scored blindly from 0 (normal) to 100 (severe injury). These results provide evidence of a role for GE in the development of HCA-induced brain injury and suggest that monosialogangliosides may have a neuroprotective effect in prolonged periods of HCA.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/G(M1) Ganglioside,
http://linkedlifedata.com/resource/pubmed/chemical/Neuroprotective Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, AMPA,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0077-8923
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
845
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
382-90
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9668371-Animals,
pubmed-meshheading:9668371-Autoradiography,
pubmed-meshheading:9668371-Brain,
pubmed-meshheading:9668371-Brain Death,
pubmed-meshheading:9668371-Cardiopulmonary Bypass,
pubmed-meshheading:9668371-Dogs,
pubmed-meshheading:9668371-G(M1) Ganglioside,
pubmed-meshheading:9668371-Heart Arrest, Induced,
pubmed-meshheading:9668371-Hypothermia, Induced,
pubmed-meshheading:9668371-Infusions, Intravenous,
pubmed-meshheading:9668371-Male,
pubmed-meshheading:9668371-Necrosis,
pubmed-meshheading:9668371-Neurons,
pubmed-meshheading:9668371-Neuroprotective Agents,
pubmed-meshheading:9668371-Receptors, AMPA,
pubmed-meshheading:9668371-Receptors, Glutamate,
pubmed-meshheading:9668371-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:9668371-Reperfusion
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pubmed:year |
1998
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pubmed:articleTitle |
The role of the monosialoganglioside, GM1 as a neuroprotectant in an experimental model of cardiopulmonary bypass and hypothermic circulatory arrest.
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pubmed:affiliation |
Johns Hopkins Hospital, Baltimore, Maryland 21287-4618, USA. WBaumgar@csurg.jhmi.jhu.edu
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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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