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- Scopus: eid_2-s2.0-0025944307
- PMID: 1742923
- WOS: WOS:A1991GM70100013
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Conference Paper: Effects of class I anti-arrhythmic drugs in infarcted tissue
Title | Effects of class I anti-arrhythmic drugs in infarcted tissue |
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Authors | |
Keywords | action potential characteristics canine Purkinje fibres class I anti-arrhythmic drugs electrophysiological effects Purkinje fibres surviving infarction rate-dependent actions |
Issue Date | 1991 |
Publisher | Canadian Medical Association. The Journal's web site is located at http://www.csci-scrc.medical.org/english/cim.html |
Citation | Clinical And Investigative Medicine, 1991, v. 14 n. 5, p. 466-475 How to Cite? |
Abstract | An in vitro model was used to examine the electrophysiological effects of anti-arrhythmic drugs in infarcted tissue. After 24 h of coronary artery occlusion in the dog, endocardial preparations were removed from the infarcted zone. Intracellulr action potentials recorded from surviving Purkinje fibres on the endocardial surface showed reduced maximum upstroke velocity (V̇(max)), increased action potential duration and enhanced automaticity. The rate-dependent effect of lidocaine on V̇(max) and conduction was more prominent in Purkinje fibres that survived myocardial infarction than in normal Purkinje fibres. Tocainide, flecainide, and O-demethyl encainide reduced V̇(max) in both normal Purkinje fibres and Purkinje fibres surviving infarction. Similar to lidocaine, these drugs showed the greatest reduction of V̇(max) in Purkinje fibres surviving infarction at the shortest stimulation cycle length tested. In contrast, maximal drug effects on action potential duration were observed when long stimulation cycle lengths were used. Our results indicate that most Class I anti-arrhythmic drugs showed rate-dependent properties in normal Purkinje fibres as well as in Purkinje fibres surviving infarction. The increased sensitivity of the ischemic myocardium to anti-arrhythmic drugs resulting in greater reductions of V̇(max) and conduction may contribute to a greater potency of anti-arrhythmic drugs in the suppression of arrhythmias associated with ischemia. Conversely, while slowing of conduction can abolish re-entry arrhythmias by producing a bidirectional block, further slowing of conduction by anti-arrhythmic drugs can favour the development of new re-entry pathways and may contribute to their pro-arrhythmic effects. |
Persistent Identifier | http://hdl.handle.net/10722/173492 |
ISSN | 2021 Impact Factor: 1.279 2020 SCImago Journal Rankings: 0.391 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Man, RYK | en_US |
dc.contributor.author | Bril, A | en_US |
dc.date.accessioned | 2012-10-30T06:32:20Z | - |
dc.date.available | 2012-10-30T06:32:20Z | - |
dc.date.issued | 1991 | en_US |
dc.identifier.citation | Clinical And Investigative Medicine, 1991, v. 14 n. 5, p. 466-475 | en_US |
dc.identifier.issn | 0147-958X | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/173492 | - |
dc.description.abstract | An in vitro model was used to examine the electrophysiological effects of anti-arrhythmic drugs in infarcted tissue. After 24 h of coronary artery occlusion in the dog, endocardial preparations were removed from the infarcted zone. Intracellulr action potentials recorded from surviving Purkinje fibres on the endocardial surface showed reduced maximum upstroke velocity (V̇(max)), increased action potential duration and enhanced automaticity. The rate-dependent effect of lidocaine on V̇(max) and conduction was more prominent in Purkinje fibres that survived myocardial infarction than in normal Purkinje fibres. Tocainide, flecainide, and O-demethyl encainide reduced V̇(max) in both normal Purkinje fibres and Purkinje fibres surviving infarction. Similar to lidocaine, these drugs showed the greatest reduction of V̇(max) in Purkinje fibres surviving infarction at the shortest stimulation cycle length tested. In contrast, maximal drug effects on action potential duration were observed when long stimulation cycle lengths were used. Our results indicate that most Class I anti-arrhythmic drugs showed rate-dependent properties in normal Purkinje fibres as well as in Purkinje fibres surviving infarction. The increased sensitivity of the ischemic myocardium to anti-arrhythmic drugs resulting in greater reductions of V̇(max) and conduction may contribute to a greater potency of anti-arrhythmic drugs in the suppression of arrhythmias associated with ischemia. Conversely, while slowing of conduction can abolish re-entry arrhythmias by producing a bidirectional block, further slowing of conduction by anti-arrhythmic drugs can favour the development of new re-entry pathways and may contribute to their pro-arrhythmic effects. | en_US |
dc.language | eng | en_US |
dc.publisher | Canadian Medical Association. The Journal's web site is located at http://www.csci-scrc.medical.org/english/cim.html | en_US |
dc.relation.ispartof | Clinical and Investigative Medicine | en_US |
dc.subject | action potential characteristics | - |
dc.subject | canine Purkinje fibres | - |
dc.subject | class I anti-arrhythmic drugs | - |
dc.subject | electrophysiological effects | - |
dc.subject | Purkinje fibres surviving infarction | - |
dc.subject | rate-dependent actions | - |
dc.subject.mesh | Action Potentials - Drug Effects | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Anti-Arrhythmia Agents - Pharmacology | en_US |
dc.subject.mesh | Disease Models, Animal | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Electrophysiology | en_US |
dc.subject.mesh | Myocardial Infarction - Physiopathology | en_US |
dc.subject.mesh | Purkinje Fibers - Drug Effects - Physiopathology | en_US |
dc.title | Effects of class I anti-arrhythmic drugs in infarcted tissue | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Man, RYK:rykman@hkucc.hku.hk | en_US |
dc.identifier.authority | Man, RYK=rp00236 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 1742923 | - |
dc.identifier.scopus | eid_2-s2.0-0025944307 | en_US |
dc.identifier.volume | 14 | en_US |
dc.identifier.issue | 5 | en_US |
dc.identifier.spage | 466 | en_US |
dc.identifier.epage | 475 | en_US |
dc.identifier.isi | WOS:A1991GM70100013 | - |
dc.publisher.place | Canada | en_US |
dc.identifier.scopusauthorid | Man, RYK=7004986435 | en_US |
dc.identifier.scopusauthorid | Bril, A=7006161753 | en_US |
dc.customcontrol.immutable | sml 170613 amended | - |
dc.identifier.issnl | 0147-958X | - |