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dc.contributor.authorKolettis, T. M.en
dc.contributor.authorBaltogiannis, G. G.en
dc.contributor.authorTsalikakis, D. G.en
dc.contributor.authorTzallas, A. T.en
dc.contributor.authorAgelaki, M. G.en
dc.contributor.authorFotopoulos, A.en
dc.contributor.authorFotiadis, D. I.en
dc.contributor.authorKyriakides, Z. S.en
dc.date.accessioned2015-11-24T19:21:21Z-
dc.date.available2015-11-24T19:21:21Z-
dc.identifier.issn0014-2999-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22096-
dc.rightsDefault Licence-
dc.subjectAction Potentials/drug effectsen
dc.subjectAnimalsen
dc.subjectAntihypertensive Agents/*pharmacologyen
dc.subjectElectrocardiographyen
dc.subjectEpinephrine/metabolismen
dc.subjectMyocardial Infarction/complications/*drug therapyen
dc.subjectNorepinephrine/metabolismen
dc.subjectRandom Allocationen
dc.subjectRatsen
dc.subjectRats, Wistaren
dc.subjectReceptor, Endothelin A/*antagonists & inhibitorsen
dc.subjectReceptor, Endothelin B/*antagonists & inhibitorsen
dc.subjectSulfonamides/*pharmacologyen
dc.subjectSympathetic Nervous System/drug effects/metabolismen
dc.subjectTachycardia, Ventricular/*drug therapy/etiologyen
dc.subjectTelemetryen
dc.subjectVentricular Fibrillation/drug therapy/etiologyen
dc.titleEffects of dual endothelin receptor blockade on sympathetic activation and arrhythmogenesis during acute myocardial infarction in ratsen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.ejphar.2007.11.002-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/18048027-
heal.identifier.secondaryhttp://ac.els-cdn.com/S001429990701240X/1-s2.0-S001429990701240X-main.pdf?_tid=4c519ae22d585db545eee9c74b2ce7fe&acdnat=1333699152_3c7f86d4c556abc8e5a855a7a7eb045f-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2008-
heal.abstractThe effects of dual (ETA and ETB) endothelin receptor blockade on ventricular arrhythmogenesis during acute myocardial infarction are not well defined. We randomly allocated Wistar rats to bosentan (100 mg/kg daily, n=24), a dual endothelin receptor antagonist, or vehicle (n=23). After 7 days of treatment, myocardial infarction was induced by permanent coronary ligation. Ventricular tachyarrhythmias were evaluated for 24 h following ligation, using a miniature telemetry electrocardiogram recorder. Action potential duration was measured from monophasic epicardial recordings and sympathetic activation was assessed by heart rate variability and catecholamine serum level measurements. Compared to controls (1012+/-185 s), bosentan (59+/-24 s) markedly decreased (P<0.00001) the total duration of ventricular tachyarrhythmias during the delayed (1-24 h) phase post-ligation, with a modest effect during the early (0-1 h) phase (132+/-38 s, versus 43+/-18 s, respectively, P=0.053). Treatment did not affect infarct size or total mortality. Action potential duration at 90% repolarization prolonged in controls (from 93.1+/-4.7 ms to 117.6+/-6.9 ms), displaying increased temporal dispersion (from 4.14+/-0.45 ms to 10.42+/-2.51 ms, both P<0.001), but was preserved in treated animals. Bosentan decreased norepinephrine, but increased epinephrine levels 24 h post-ligation. Low frequency spectra of heart rate variability, an index of net sympathetic tone, were lower in bosentan-treated rats. Dual endothelin-1 receptor blockade decreases ventricular tachyarrhythmias during myocardial infarction without reperfusion, by preventing repolarization inhomogeneity. Diverse treatment effects on sympathetic activation may ameliorate the antiarrhythmic action.en
heal.journalNameEuropean Journal of Pharmacologyen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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