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Article: Effects of quinidine on arrhythmias and conduction in an isolated tissue model of ischemia and reperfusion

TitleEffects of quinidine on arrhythmias and conduction in an isolated tissue model of ischemia and reperfusion
Authors
Issue Date1991
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1991, v. 17 n. 2, p. 239-248 How to Cite?
AbstractTransmembrane electrical activity from endo- and epicardium and a high-gain ECG were recorded from isolated segments of guinea pig right ventricles. Endocardium was stimulated. Tissues were exposed to ischemic conditions for 15 min and then reperfused with ''normal'' Tyrode's solution. Ventricular tachycardia, bigeminy, or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 68% of control hearts. Arrhythmias were associated with prolongation of the transmural conduction time (CT) and abbreviation of the endocardial effective refractory period (EP). Quinidine significantly suppressed reperfusion arrhythmias at 1 and 5 μM, slightly increased the incidence of arrhythmias at 10 μM, and again suppressed arrhythmias at 50 and 100 μM. At 1 and 5 μM, quinidine prevented or attenuated prolongation of the transmural CT by ischemic conditions and reperfusion. The transmural CT was not significantly changed at 10 μM, and was further prolonged at 50 and 100 μM quinidine. The endocardial ERP was prolonged by 50 and 100 μM quinidine during ischemic conditions and reperfusion. In epicardial slices, 5 μM quinidine shortened the CT transverse to the fiber orientation during reperfusion but had no effect on the longitudinal CT. Thus, antiarrhythmic efficacy of low concentrations of quinidine may occur through differential effects dependent on tissue anisotropy.
Persistent Identifierhttp://hdl.handle.net/10722/161887
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_US
dc.contributor.authorFerrier, GRen_US
dc.date.accessioned2012-09-05T05:15:49Z-
dc.date.available2012-09-05T05:15:49Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1991, v. 17 n. 2, p. 239-248en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/161887-
dc.description.abstractTransmembrane electrical activity from endo- and epicardium and a high-gain ECG were recorded from isolated segments of guinea pig right ventricles. Endocardium was stimulated. Tissues were exposed to ischemic conditions for 15 min and then reperfused with ''normal'' Tyrode's solution. Ventricular tachycardia, bigeminy, or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 68% of control hearts. Arrhythmias were associated with prolongation of the transmural conduction time (CT) and abbreviation of the endocardial effective refractory period (EP). Quinidine significantly suppressed reperfusion arrhythmias at 1 and 5 μM, slightly increased the incidence of arrhythmias at 10 μM, and again suppressed arrhythmias at 50 and 100 μM. At 1 and 5 μM, quinidine prevented or attenuated prolongation of the transmural CT by ischemic conditions and reperfusion. The transmural CT was not significantly changed at 10 μM, and was further prolonged at 50 and 100 μM quinidine. The endocardial ERP was prolonged by 50 and 100 μM quinidine during ischemic conditions and reperfusion. In epicardial slices, 5 μM quinidine shortened the CT transverse to the fiber orientation during reperfusion but had no effect on the longitudinal CT. Thus, antiarrhythmic efficacy of low concentrations of quinidine may occur through differential effects dependent on tissue anisotropy.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAction Potentials - Drug Effectsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArrhythmias, Cardiac - Etiology - Physiopathologyen_US
dc.subject.meshCoronary Disease - Complications - Physiopathologyen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart Conduction System - Drug Effectsen_US
dc.subject.meshMyocardial Reperfusion Injury - Physiopathologyen_US
dc.subject.meshQuinidine - Pharmacologyen_US
dc.subject.meshVentricular Function, Right - Drug Effectsen_US
dc.titleEffects of quinidine on arrhythmias and conduction in an isolated tissue model of ischemia and reperfusionen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-199102000-00009-
dc.identifier.pmid1709228-
dc.identifier.scopuseid_2-s2.0-0025972947en_US
dc.identifier.volume17en_US
dc.identifier.issue2en_US
dc.identifier.spage239en_US
dc.identifier.epage248en_US
dc.identifier.isiWOS:A1991EU56100009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridFerrier, GR=7005858840en_US

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