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Article: Electrophysiological effects of acetylcholine in Purkinje fibres surviving infarction

TitleElectrophysiological effects of acetylcholine in Purkinje fibres surviving infarction
Authors
Issue Date1990
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 1990, v. 24 n. 4, p. 296-302 How to Cite?
AbstractStudy objective - The aim of the study was to investigate the electrophysiological effects of acetylcholine in Purkinje fibres surviving infarction. Design - Infarction in canine hearts was produced by coronary occlusion. Ischaemic tissue was removed and surviving Purkinje fibres were compared for effects of increasing concentrations of acetylcholine (1-100 μM) with control Purkinje fibres from normal hearts and normal Purkinje fibres treated with barium. Subjects - Experimental animals were mongrel dogs of either sex, weight 10-15 kg, n = 14 (control), 9 (infarction group), 11 (Ba treated group). Measurements and main results - Acetylcholine caused concentration dependent shortening of action potential duration in normal Purkinje fibres and in fibres surviving infarction, but had no effect when potassium conductance was decreases with Ba. Acetylcholine induced a small hyperpolarisation in normal Purkinje fibres and in fibres surviving infarction perfused with a 4 mM potassium solution without affecting action potential amplitude or dV/dt(max). Reduction in K concentration to 1 and 2 mM caused a greater depolarisation of diastolic potential in normal fibres than in fibres surviving infarction or Ba treated fibres. Acetylcholine produced hyperpolarisation under these conditions in normal fibres only. Acetylcholine decreased automaticity in normal fibres only at high concentration (100 μM). A lesser effect was seen in Ba treated fibres and in fibres surviving infarction. Conclusions - Since Ba treated Purkinje fibres had similar action potential characteristics to those seen in Purkinje fibres surviving infarction and responded in the same way to the modifications of K concentration, a decrease in K conductance might be the underlying mechanism for some of the electrophysiological changes in fibres surviving infarction. The results also suggest that after 24 h ischaemia, surviving Purkinje fibres have a different sensitivity to acetylcholine from normal fibres.
Persistent Identifierhttp://hdl.handle.net/10722/170986
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBril, Aen_US
dc.contributor.authorMan, RYKen_US
dc.date.accessioned2012-10-30T06:11:43Z-
dc.date.available2012-10-30T06:11:43Z-
dc.date.issued1990en_US
dc.identifier.citationCardiovascular Research, 1990, v. 24 n. 4, p. 296-302en_US
dc.identifier.issn0008-6363en_US
dc.identifier.urihttp://hdl.handle.net/10722/170986-
dc.description.abstractStudy objective - The aim of the study was to investigate the electrophysiological effects of acetylcholine in Purkinje fibres surviving infarction. Design - Infarction in canine hearts was produced by coronary occlusion. Ischaemic tissue was removed and surviving Purkinje fibres were compared for effects of increasing concentrations of acetylcholine (1-100 μM) with control Purkinje fibres from normal hearts and normal Purkinje fibres treated with barium. Subjects - Experimental animals were mongrel dogs of either sex, weight 10-15 kg, n = 14 (control), 9 (infarction group), 11 (Ba treated group). Measurements and main results - Acetylcholine caused concentration dependent shortening of action potential duration in normal Purkinje fibres and in fibres surviving infarction, but had no effect when potassium conductance was decreases with Ba. Acetylcholine induced a small hyperpolarisation in normal Purkinje fibres and in fibres surviving infarction perfused with a 4 mM potassium solution without affecting action potential amplitude or dV/dt(max). Reduction in K concentration to 1 and 2 mM caused a greater depolarisation of diastolic potential in normal fibres than in fibres surviving infarction or Ba treated fibres. Acetylcholine produced hyperpolarisation under these conditions in normal fibres only. Acetylcholine decreased automaticity in normal fibres only at high concentration (100 μM). A lesser effect was seen in Ba treated fibres and in fibres surviving infarction. Conclusions - Since Ba treated Purkinje fibres had similar action potential characteristics to those seen in Purkinje fibres surviving infarction and responded in the same way to the modifications of K concentration, a decrease in K conductance might be the underlying mechanism for some of the electrophysiological changes in fibres surviving infarction. The results also suggest that after 24 h ischaemia, surviving Purkinje fibres have a different sensitivity to acetylcholine from normal fibres.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_US
dc.relation.ispartofCardiovascular Researchen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAction Potentials - Drug Effectsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBarium - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshFemaleen_US
dc.subject.meshHeart Conduction System - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMyocardial Infarction - Physiopathologyen_US
dc.subject.meshPurkinje Fibers - Drug Effects - Physiopathologyen_US
dc.titleElectrophysiological effects of acetylcholine in Purkinje fibres surviving infarctionen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/cvr/24.4.296-
dc.identifier.pmid2346965-
dc.identifier.scopuseid_2-s2.0-0025274936en_US
dc.identifier.volume24en_US
dc.identifier.issue4en_US
dc.identifier.spage296en_US
dc.identifier.epage302en_US
dc.identifier.isiWOS:A1990CZ13000006-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridBril, A=7006161753en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US

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