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Article: Acute and chronic effects of dexfenfluramine on the porcine coronary artery

TitleAcute and chronic effects of dexfenfluramine on the porcine coronary artery
Authors
Issue Date1996
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1996, v. 279 n. 3, p. 1077-1085 How to Cite?
AbstractExperiments were designed to verify whether or not acute or chronic exposure to dexfenfluramine favors the occurrence of coronary vasospasm in vivo or in vitro. Rings of left anterior and left circumflex porcine coronary artery, with and without endothelium, were studied in conventional organ chambers for the measurement of isometric force. The donor pigs were divided into two groups: controls and animals fed for 4 weeks with dexfenfluramine. In each group, one-half of the animals underwent balloon denudation of the left anterior descending coronary artery at the beginning of the study. Coronary angiography was performed at the time of denudation and, in all animals, during the 3rd week of the study. Acutely, dexfenfluramine at concentrations higher than 10 5 M caused contractions which were blunted by the presence of the endothelium and inhibited by indomethacin (an inhibitor of cyclooxygenase). Chronic treatment with dexfenfluramine did not affect coronary diameter and did not after the response to intracoronary infusion of serotonin. Chronic treatment with dexfenfluramine reduced the contractions of rings without endothelium to serotonin, but not those to norepinephrine or endothelin. It did not affect endothelium-dependent relaxations in the absence or presence of pertussis toxin to serotonin, UK14304 (alpha-2 adrenergic agonist), adenosine diphosphate or aggregating platelets. Chronic treatment with dexfenfluramine did not modify relaxations of rings without endothelium to SIN-1 (nitric oxide donor; the active metabolite of molsidomine) or adenosine diphosphate. These findings do not support the hypothesis that acute or chronic exposure to dexfenfluramine favors the occurrence of coronary vasospasm.
Persistent Identifierhttp://hdl.handle.net/10722/171194
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDesta, Ben_US
dc.contributor.authorSchultz, Den_US
dc.contributor.authorRavel, Den_US
dc.contributor.authorLaudignon, Nen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBoulanger, CMen_US
dc.date.accessioned2012-10-30T06:12:37Z-
dc.date.available2012-10-30T06:12:37Z-
dc.date.issued1996en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1996, v. 279 n. 3, p. 1077-1085en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171194-
dc.description.abstractExperiments were designed to verify whether or not acute or chronic exposure to dexfenfluramine favors the occurrence of coronary vasospasm in vivo or in vitro. Rings of left anterior and left circumflex porcine coronary artery, with and without endothelium, were studied in conventional organ chambers for the measurement of isometric force. The donor pigs were divided into two groups: controls and animals fed for 4 weeks with dexfenfluramine. In each group, one-half of the animals underwent balloon denudation of the left anterior descending coronary artery at the beginning of the study. Coronary angiography was performed at the time of denudation and, in all animals, during the 3rd week of the study. Acutely, dexfenfluramine at concentrations higher than 10 5 M caused contractions which were blunted by the presence of the endothelium and inhibited by indomethacin (an inhibitor of cyclooxygenase). Chronic treatment with dexfenfluramine did not affect coronary diameter and did not after the response to intracoronary infusion of serotonin. Chronic treatment with dexfenfluramine reduced the contractions of rings without endothelium to serotonin, but not those to norepinephrine or endothelin. It did not affect endothelium-dependent relaxations in the absence or presence of pertussis toxin to serotonin, UK14304 (alpha-2 adrenergic agonist), adenosine diphosphate or aggregating platelets. Chronic treatment with dexfenfluramine did not modify relaxations of rings without endothelium to SIN-1 (nitric oxide donor; the active metabolite of molsidomine) or adenosine diphosphate. These findings do not support the hypothesis that acute or chronic exposure to dexfenfluramine favors the occurrence of coronary vasospasm.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBody Weighten_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshFenfluramine - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPlatelet Aggregation - Drug Effectsen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleAcute and chronic effects of dexfenfluramine on the porcine coronary arteryen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8968327en_US
dc.identifier.scopuseid_2-s2.0-0030438453en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030438453&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume279en_US
dc.identifier.issue3en_US
dc.identifier.spage1077en_US
dc.identifier.epage1085en_US
dc.identifier.isiWOS:A1996VY20700003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridDesta, B=6603788474en_US
dc.identifier.scopusauthoridSchultz, D=7202619693en_US
dc.identifier.scopusauthoridRavel, D=6602456375en_US
dc.identifier.scopusauthoridLaudignon, N=6701446865en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US

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