Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22396
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dc.contributor.authorOikonomidis, D. L.en
dc.contributor.authorBaltogiannis, G. G.en
dc.contributor.authorKolettis, T. M.en
dc.date.accessioned2015-11-24T19:23:59Z-
dc.date.available2015-11-24T19:23:59Z-
dc.identifier.issn1572-8595-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22396-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectCoronary Occlusion/complications/physiopathologyen
dc.subjectEndothelin-1/blood/physiologyen
dc.subjectHumansen
dc.subjectMyocardial Infarction/blood/*complications/etiology/pathology/physiopathologyen
dc.subjectReceptor, Endothelin A/drug effects/physiologyen
dc.subjectReceptor, Endothelin B/drug effects/physiologyen
dc.subjectReceptors, Endothelin/*drug effectsen
dc.subjectSignal Transduction/physiologyen
dc.subjectSympathetic Nervous System/physiopathologyen
dc.subjectTachycardia, Ventricular/physiopathology/prevention & controlen
dc.titleDo endothelin receptor antagonists have an antiarrhythmic potential during acute myocardial infarction? Evidence from experimental studiesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1007/s10840-010-9493-5-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/20532602-
heal.identifier.secondaryhttp://www.springerlink.com/content/2068701781834252/fulltext.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2010-
heal.abstractSudden cardiac death constitutes a major health-related problem. In the majority of cases, sudden cardiac death is due to ventricular tachyarrhythmias secondary to acute myocardial infarction. The pathophysiologic chain of events leading to ventricular tachyarrhythmias after acute coronary occlusion is complex and incompletely understood. Experimental and clinical studies have indicated that endothelin-1 production rises markedly very early in the course of myocardial infarction. Endothelin-1 exerts significant electrophysiologic actions on ventricular cardiomyocytes and participates in the genesis of ischemic ventricular tachyarrhythmias. Endothelin-1, acting via two G-protein-coupled receptors (ETA and ETB), prolongs the action potential duration and increases the occurrence of spontaneous calcium transients, resulting in early afterdepolarizations and ventricular tachyarrhythmias via triggered activity. Moreover, endothelin-1 enhances sympathetic stimulation, a well established contributor to ventricular arrhythmogenesis during acute myocardial infarction. Despite these considerations, the therapeutic potential of endothelin receptor antagonists as antiarrhythmic drugs during myocardial ischemia/infarction is still under investigation. To date, a number of endothelin-1 receptor antagonists are available, presenting different degrees of selectivity for ETA and ETB receptors. The arrhythmogenic effects of endothelin-1 are exerted mainly via stimulation of the ETA receptors, but the role of ETB receptors remains controversial, as previous studies have produced conflicting results. This review summarizes the current state-of-the-art on the role of endothelin-1 in the genesis of ventricular arrhythmias during acute myocardial infarction and raises some hypotheses that could be explored in future studies.en
heal.journalNameJ Interv Card Electrophysiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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