Source:http://linkedlifedata.com/resource/pubmed/id/15085069
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2004-4-15
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pubmed:abstractText |
Methotrexate, an anti-rheumatic agent, has recently been reported to show an anti-inflammatory action via ecto-5'-nucleotidase- and adenosine-dependent mechanisms. Because ecto-5'-nucleotidase contributes to the production of adenosine and adenosine has a potent cardioprotective effect against ischemia/reperfusion injury, we investigated whether methotrexate or MX-68 [N-1-((2,4-diamino-6-pteridinyl) methyl)-3,4-dihydro-2H-1,4-benzothiazine-7- carbonyl]-N-2- aminoadipic acid] could reduce infarct size via adenosine-dependent mechanisms. In beagle dogs, the left anterior descending coronary artery was perfused through a bypass tube, which was occluded for 90 minutes followed by 6 hours of reperfusion. The size of infarcts was assessed by TTC staining. MX-68 reduced infarct size compared with that in untreated dogs (13.7 +/- 1.9 versus 38.6 +/- 5.3%, P < 0.01). This effect was completely blunted by either the adenosine receptor antagonist 8-sulfophenyltheophylline (8-SPT) (45.0 +/- 4.6% and 46.8 +/- 5.8% in the 8-SPT and MX-68 + 8-SPT groups, respectively) or by the ecto-5'-nucleotidase inhibitoralpha,beta-methylenadenosine 5'-diphosphate (AMP-CP) (44.0 +/- 4.5% and 46.7 +/- 5.8% in the AMP-CP and MX-68 + AMP-CP groups, respectively). Methotrexate also reduced infarct size to a level comparable with that in the MX-68 group, and its effect was also blunted by 8-SPT. There were no significant differences of collateral blood flow or risk area between the groups. We conclude that methotrexate and its derivative (MX-68) both limit infarct size via adenosine-dependent mechanisms.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-Aminoadipic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/8-(4-sulfophenyl)theophylline,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Methotrexate,
http://linkedlifedata.com/resource/pubmed/chemical/N-(1-((2,4-diamino-6-pteridinyl)meth...,
http://linkedlifedata.com/resource/pubmed/chemical/Purinergic P1 Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Purinergic P1,
http://linkedlifedata.com/resource/pubmed/chemical/Theophylline
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0160-2446
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pubmed:author |
pubmed-author:AsakuraMasanoriM,
pubmed-author:AsanumaHiroshiH,
pubmed-author:HoriMasatsuguM,
pubmed-author:KitakazeMasafumiM,
pubmed-author:MinaminoTetsuoT,
pubmed-author:MoriHidezoH,
pubmed-author:NodeKoichiK,
pubmed-author:OgaiAkikoA,
pubmed-author:OgitaHisakazuH,
pubmed-author:SanadaShojiS,
pubmed-author:ShinozakiYoshiroY,
pubmed-author:TakashimaSeijiS,
pubmed-author:TomoikeHitonobuH
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pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
574-9
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15085069-2-Aminoadipic Acid,
pubmed-meshheading:15085069-Adenosine,
pubmed-meshheading:15085069-Animals,
pubmed-meshheading:15085069-Cardiotonic Agents,
pubmed-meshheading:15085069-Dogs,
pubmed-meshheading:15085069-Methotrexate,
pubmed-meshheading:15085069-Myocardial Infarction,
pubmed-meshheading:15085069-Purinergic P1 Receptor Antagonists,
pubmed-meshheading:15085069-Receptors, Purinergic P1,
pubmed-meshheading:15085069-Theophylline
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pubmed:year |
2004
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pubmed:articleTitle |
Methotrexate and MX-68, a new derivative of methotrexate, limit infarct size via adenosine-dependent mechanisms in canine hearts.
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pubmed:affiliation |
Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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