Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/21963
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dc.contributor.authorOikonomidis, D. L.en
dc.contributor.authorTsalikakis, D. G.en
dc.contributor.authorBaltogiannis, G. G.en
dc.contributor.authorTzallas, A. T.en
dc.contributor.authorXourgia, X.en
dc.contributor.authorAgelaki, M. G.en
dc.contributor.authorMegalou, A. J.en
dc.contributor.authorFotopoulos, A.en
dc.contributor.authorPapalois, A.en
dc.contributor.authorKyriakides, Z. S.en
dc.contributor.authorKolettis, T. M.en
dc.date.accessioned2015-11-24T19:19:28Z-
dc.date.available2015-11-24T19:19:28Z-
dc.identifier.issn1435-1803-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21963-
dc.rightsDefault Licence-
dc.subjectAction Potentialsen
dc.subjectAdrenergic beta-Antagonists/therapeutic useen
dc.subjectAnimalsen
dc.subjectCatecholamines/blooden
dc.subjectElectrocardiographyen
dc.subjectHeart Rateen
dc.subjectMyocardial Infarction/complications/*metabolism/pathology/physiopathologyen
dc.subjectMyocardium/pathologyen
dc.subjectRatsen
dc.subjectReceptor, Endothelin B/genetics/*metabolismen
dc.subjectTachycardia, Ventricular/etiology/*metabolism/prevention & controlen
dc.subjectVentricular Dysfunction, Leften
dc.subjectVentricular Fibrillation/etiology/*metabolism/prevention & controlen
dc.titleEndothelin-B receptors and ventricular arrhythmogenesis in the rat model of acute myocardial infarctionen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1007/s00395-009-0066-7-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/19838761-
heal.identifier.secondaryhttp://www.springerlink.com/content/bh864857273m070g/fulltext.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2010-
heal.abstractThe arrhythmogenic effects of endothelin-1 (ET-1) are mediated via ETA-receptors, but the role of ETB-receptors is unclear. We examined the pathophysiologic role of ETB-receptors on ventricular tachyarrhythmias (VT/VF) during myocardial infarction (MI). MI was induced by coronary ligation in two animal groups, namely in wild-type (n = 63) and in ETB-receptor-deficient (n = 61) rats. Using a telemetry recorder, VT/VF episodes were evaluated during phase I (the 1st hour) and phase II (2-24 h) post-MI, with and without prior beta-blockade. Action potential duration at 90% repolarization (APD90) was measured from monophasic epicardial recordings and indices of sympathetic activation were assessed using fast-Fourier analysis of heart rate variability. Serum epinephrine and norepinephrine were measured with radioimmunoassay. MI size was similar in the two groups. There was a marked temporal variation in VT/VF duration; during phase I, it was higher (p = 0.0087) in ETB-deficient (1,519 +/- 421 s) than in wild-type (190 +/- 34 s) rats, but tended (p = 0.086) to be lower in ETB-deficient (4.2 +/- 2.0 s) than in wild-type (27.7 +/- 8.0 s) rats during phase II. Overall, the severity of VT/VF was greater in ETB-deficient rats, evidenced by higher (p = 0.0058) mortality (72.0% vs. 32.1%). There was a temporal variation in heart rate and in the ratio of low- to high-frequency spectra, being higher (<0.001) during phase I, but lower (p < 0.05) during phase II in ETB-deficient rats. Likewise, 1 h post-MI, serum epinephrine (p = 0.025) and norepinephrine (p < 0.0001) were higher in ETB-deficient (4.20 +/- 0.54, 14.24 +/- 1.39 ng/ml) than in wild-type (2.30 +/- 0.59, 5.26 +/- 0.67 ng/ml) rats, respectively. After beta-blockade, VT/VF episodes and mortality were similar in the two groups. The ETB-receptor decreases sympathetic activation and arrhythmogenesis during the early phase of MI, but these effects diminish during evolving MI.en
heal.journalNameBasic Res Cardiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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