Source:http://linkedlifedata.com/resource/pubmed/id/12798419
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
2003-6-11
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| pubmed:abstractText |
The effects of the selective delta-1 (delta(1)) opioid receptor agonist, DPDPE, and the selective delta(2) opioid receptor agonist, DSLET, have been studied on the ventricular fibrillation threshold (VFT) in rats with an experimental post-infarction cardiosclerosis (CS). It has been found that CS induced a significant decrease in VFT. This CS-induced decrease in VFT was significantly reversed by intravenous administration of DPDPE (0.1 mg/kg) 10 min before VFT measurement. On the contrary, intravenous injection of DSLET (0.5 mg/kg) exacerbated the CS-induced cardiac electrical instability. Pretreatment with the selective delta opioid receptor antagonist, ICI 174,864 (0.5 mg/kg), completely abolished the changes in VFT produced by both DPDPE and DSLET. Previous administration of a nonselective peripherally acting opioid receptor antagonist, naloxone methiodide (5 mg/kg) also completely reversed the antifibrillatory action of DPDPE. Naloxone methiodide and ICI 174,864 alone had no effect on VFT. Pretreatment with the nonselective K(ATP) channel blocker, glibenclamide (0.3 mg/kg), or with the mitochondrial selective K(ATP) channel blocker, 5-hydroxydecanoic acid (5-HD, 5 mg/kg), completely abolished the DPDPE-induced increase in cardiac electrical stability. Glibenclamide and 5-HD alone had no effect on VFT. These results demonstrate that the delta opioid receptor plays an important role in the regulation of electrical stability in rats with post-infarction cardiosclerosis. We propose that peripheral delta(1) opioid receptor stimulation reverses CS-induced electrical instability via mitochondrial K(ATP) channels. On the contrary, delta(2) opioid receptor stimulation may exacerbate the CS-induced decrease in VFT. Further studies are necessary to determine the delta opioid receptor subtype which mediates the antifibrillatory effect of DPDPE and pro-fibrillatory effect of DSLET.
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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/5-hydroxydecanoic acid,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Analgesics, Opioid,
http://linkedlifedata.com/resource/pubmed/chemical/Decanoic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, D-Penicillamine (2,5)-,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, Leucine,
http://linkedlifedata.com/resource/pubmed/chemical/Glyburide,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxy Acids,
http://linkedlifedata.com/resource/pubmed/chemical/N,N-diallyl-tyrosyl-alpha-aminoisobu...,
http://linkedlifedata.com/resource/pubmed/chemical/N-methylnaloxone,
http://linkedlifedata.com/resource/pubmed/chemical/Naloxone,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Quaternary Ammonium Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, delta,
http://linkedlifedata.com/resource/pubmed/chemical/enkephalin, Ser(2), Leu(5), Thr(6)-
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0024-3205
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
4
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| pubmed:volume |
73
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
947-52
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:12798419-Adenosine Triphosphate,
pubmed-meshheading:12798419-Analgesics, Opioid,
pubmed-meshheading:12798419-Animals,
pubmed-meshheading:12798419-Decanoic Acids,
pubmed-meshheading:12798419-Disease Models, Animal,
pubmed-meshheading:12798419-Drug Antagonism,
pubmed-meshheading:12798419-Enkephalin, D-Penicillamine (2,5)-,
pubmed-meshheading:12798419-Enkephalin, Leucine,
pubmed-meshheading:12798419-Glyburide,
pubmed-meshheading:12798419-Hydroxy Acids,
pubmed-meshheading:12798419-Male,
pubmed-meshheading:12798419-Mitochondria, Heart,
pubmed-meshheading:12798419-Myocardial Infarction,
pubmed-meshheading:12798419-Myocardium,
pubmed-meshheading:12798419-Naloxone,
pubmed-meshheading:12798419-Potassium Channels,
pubmed-meshheading:12798419-Quaternary Ammonium Compounds,
pubmed-meshheading:12798419-Rats,
pubmed-meshheading:12798419-Rats, Wistar,
pubmed-meshheading:12798419-Receptors, Opioid, delta,
pubmed-meshheading:12798419-Sclerosis,
pubmed-meshheading:12798419-Ventricular Fibrillation
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| pubmed:year |
2003
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| pubmed:articleTitle |
Activation of peripheral delta opioid receptors eliminates cardiac electrical instability in a rat model of post-infarction cardiosclerosis via mitochondrial ATP-dependent K+ channels.
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| pubmed:affiliation |
Laboratory of Experimental Cardiology, Institute of Cardiology, 634050 Tomsk, Russia.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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