Endothelin receptor--a blockade decreases ventricular arrhythmias after myocardial infarction in rats

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dc.contributor.authorBaltogiannis, G. G.en
dc.contributor.authorTsalikakis, D. G.en
dc.contributor.authorMitsi, A. C.en
dc.contributor.authorHatzistergos, K. E.en
dc.contributor.authorElaiopoulos, D.en
dc.contributor.authorFotiadis, D. I.en
dc.contributor.authorKyriakides, Z. S.en
dc.contributor.authorKolettis, T. M.en
dc.date.accessioned2015-11-24T19:19:31Z
dc.date.available2015-11-24T19:19:31Z
dc.identifier.issn0008-6363-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21966
dc.rightsDefault Licence-
dc.subjectAction Potentials/drug effectsen
dc.subjectAnimalsen
dc.subjectArrhythmias, Cardiac/*drug therapy/etiology/physiopathologyen
dc.subjectElectrocardiography, Ambulatoryen
dc.subjectFemaleen
dc.subjectMyocardial Infarction/complications/*drug therapy/physiopathologyen
dc.subjectPeptides, Cyclic/*therapeutic useen
dc.subjectRandom Allocationen
dc.subjectRatsen
dc.subjectRats, Wistaren
dc.subjectReceptor, Endothelin A/*antagonists & inhibitorsen
dc.subjectTachycardia, Ventricular/drug therapy/physiopathologyen
dc.subjectTelemetry/methodsen
dc.subjectVentricular Fibrillation/drug therapy/physiopathologyen
dc.titleEndothelin receptor--a blockade decreases ventricular arrhythmias after myocardial infarction in ratsen
heal.abstractOBJECTIVE: Endothelin-1 (ET-1) production increases during acute myocardial infarction (MI) and may contribute to the genesis of ventricular tachycardia (VT) and ventricular fibrillation (VF). However, the antiarrhythmic effects of ET-1 receptor blockade, examined shortly after MI, have been debated. In the present study, we examined the effects of such treatment on VT/VF during the first 24 h post-MI. METHODS: Thirty-five Wistar rats (223+/-22 g) were randomly allocated to either the ET-1 receptor-A (ETA) antagonist BQ-123 (0.4 mg/kg, BQ-123 group, n=17), or normal saline (control group, n=18) and were subjected to coronary artery ligation. A single-lead electrocardiogram was continuously recorded for 24 h post-MI, using an implanted telemetry system, and episodes of VT/VF were analyzed. Monophasic action potential (MAP) recordings were obtained from the left (LV) and right (RV) ventricular epicardium at baseline, 5 min after treatment and 24 h post-MI. RESULTS: There were 15.94+/-19.35 episodes/h/rat of VT/VF in the control group and 1.66+/-2.22 in the BQ-123 group (p=0.010), resulting in a lower (p=0.030) arrhythmic mortality in treated animals. The mean episode duration was 7.40+/-7.16 s for the control group and 2.30+/-1.37 s for the BQ-123 group (p=0.011). The maximum decrease in VT/VF was observed during the 1st, 5th and 6th hours post-MI. In the control group, LV MAP duration increased 24 h post-MI, displaying an increased beat-to-beat variation, but remained unchanged in the BQ-123 group. CONCLUSION: Acute ETA blockade reduces the incidence of VT/V F during the first 24-h post-MI in the rat, through a decrease in the dispersion of repolarization.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.primary10.1016/j.cardiores.2005.04.020-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15907816-
heal.identifier.secondaryhttp://cardiovascres.oxfordjournals.org/content/67/4/647.full.pdf-
heal.journalNameCardiovasc Resen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2005-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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