Effect of adrenergic blockade on pressure-related ventricular arrhythmias

dc.contributor.authorSideris, D. A.en
dc.contributor.authorToumanidis, S. T.en
dc.contributor.authorKostis, E. B.en
dc.contributor.authorSpyropoulos, G.en
dc.contributor.authorMoulopoulos, S. D.en
dc.date.accessioned2015-11-24T19:23:06Z
dc.date.available2015-11-24T19:23:06Z
dc.identifier.issn0001-5385-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22248
dc.rightsDefault Licence-
dc.subjectAdrenergic beta-Antagonists/*pharmacology/therapeutic useen
dc.subjectAnimalsen
dc.subjectArrhythmias, Cardiac/drug therapy/*physiopathologyen
dc.subjectDogsen
dc.subjectHypertension/drug therapy/*physiopathologyen
dc.subjectVentricular Function/*drug effects/physiologyen
dc.titleEffect of adrenergic blockade on pressure-related ventricular arrhythmiasen
heal.abstractThis paper examines whether adrenergic blockade (B1) may prevent the arrhythmogenic effect of acute arterial pressure (AP) elevation. In 7 anesthetized dogs iv propranolol (0.2 mg/kg) was given and in another 2 dogs stellate ganglion excision was performed. Before and after these B1 manoeuvres the AP was repeatedly increased by either elevating an open-air arterial pressure reservoir or administering iv metaraminol and decreased by abating the pressure reservoir. In a continuous recording of AP and ECG the systolic (S) AP and the presence (or absence) of ventricular arrhythmia (A) was noted. Before B1 A was noted in 652/1715 (38.0%) 5-sec periods at a SAP of 160.3 +/- 69.9 mm Hg which was significantly higher than in the 1063 5-sec periods without A (104.2 +/- 54.3) in all experiments. Following B1 it was impossible to cause A in 3 experiments. In the remaining experiments the A incidence was reduced (significantly in 5/9 experiments) to a total of 253/983 (25.7%) periods (P less than 0.001). In the 5/9 experiments with post-B1 A, the mean SAP was higher with (185.0 +/- 97.9 mm Hg) than without A (113.7 +/- 59.9 mm Hg) (significantly in 2/9 experiments). Following fitting of the SAP distributions before and after B1 to their common distribution (i.e. the same AP), the incidence of A was higher before than after B1 in all experiments (significantly in 7/9). It is concluded that B1 has an antiarrhythmic action on AP-related A. This antiarrhythmic effect seems to be due partly to an antihypertensive effect of B1 and partly to an antiarrhythmic effect of B1 for a given AP.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/1675514-
heal.journalNameActa Cardiolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate1991-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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