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Article: Modification of excitation-contraction coupling in cat ventricular myocardium following endocardial damage

TitleModification of excitation-contraction coupling in cat ventricular myocardium following endocardial damage
Authors
Issue Date1993
PublisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjpp
Citation
Canadian Journal Of Physiology And Pharmacology, 1993, v. 71 n. 3-4, p. 254-262 How to Cite?
AbstractDamage to endocardial endothelium (denudation of the superficial tissue) by brief exposure to a 100-μL bolus of detergent (Triton X-100, 1% by volume stock) decreased the twitch force of papillary muscle (and trabeculae) by ~30% to a new but steady level without changes in resting tension. The decline in twitch force was evident immediately after the addition of Triton. Modification of the action potential measured from the contracting tissue appeared only later, when the change in contraction was already well established (i.e., after ~2 min). Action potential shortened in duration at 50% repolarization by ~100 ms and increased in plateau amplitude, although the latter increase was not always observed. A similar treatment procedure applied to strips of ventricular wall with the endocardium exposed to the superfusion solution resulted in a substantial decrease in action potential duration (~110 ms). In contrast, treatment of strips of epicardial layers of ventricular walls (with epicardial side facing the superfusion solution) did not produce a similar result. In β-stimulated (1 μM isoproterenol) and partially depolarized preparations (with 20 mM KCl), with intact endocardium, electrically evoked contractions were followed by aftercontractions, which were suppressed following Triton treatment. Action potentials in a depolarizing medium also shortened in duration (~50 ms), although following a delay (2-3 min). The decay to steady state of postextrasystolic potentiated beat was slower after endocardial damage than under control conditions. This suggested an increased Ca2+ recirculation through the sarcoplasmic reticulum between two consecutive beats (35% before Triton vs. 45% after Triton). Finally, in a medium containing 3 μM ryanodine, Triton treatment of the endocardial endothelium failed to induce any effect on either twitch force or action potential. Prolonged exposure to Triton X-100 (by a slow flow or high concentration) induced only deteriorating effects leading to substantial rise in the resting tension and generation of contractures and abbreviated action potentials with depressed plateau. These observations are consistent with the hypothesis that a modification in the sarcoplasmic reticulum function may, at least in part, be responsible for the observed changes in contractile function of the myocardium following endocardial damage with Triton treatment.
Persistent Identifierhttp://hdl.handle.net/10722/171577
ISSN
2015 Impact Factor: 1.704
2015 SCImago Journal Rankings: 0.683
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorBanijamali, HSen_US
dc.contributor.authorChallice, CEen_US
dc.date.accessioned2012-10-30T06:15:47Z-
dc.date.available2012-10-30T06:15:47Z-
dc.date.issued1993en_US
dc.identifier.citationCanadian Journal Of Physiology And Pharmacology, 1993, v. 71 n. 3-4, p. 254-262en_US
dc.identifier.issn0008-4212en_US
dc.identifier.urihttp://hdl.handle.net/10722/171577-
dc.description.abstractDamage to endocardial endothelium (denudation of the superficial tissue) by brief exposure to a 100-μL bolus of detergent (Triton X-100, 1% by volume stock) decreased the twitch force of papillary muscle (and trabeculae) by ~30% to a new but steady level without changes in resting tension. The decline in twitch force was evident immediately after the addition of Triton. Modification of the action potential measured from the contracting tissue appeared only later, when the change in contraction was already well established (i.e., after ~2 min). Action potential shortened in duration at 50% repolarization by ~100 ms and increased in plateau amplitude, although the latter increase was not always observed. A similar treatment procedure applied to strips of ventricular wall with the endocardium exposed to the superfusion solution resulted in a substantial decrease in action potential duration (~110 ms). In contrast, treatment of strips of epicardial layers of ventricular walls (with epicardial side facing the superfusion solution) did not produce a similar result. In β-stimulated (1 μM isoproterenol) and partially depolarized preparations (with 20 mM KCl), with intact endocardium, electrically evoked contractions were followed by aftercontractions, which were suppressed following Triton treatment. Action potentials in a depolarizing medium also shortened in duration (~50 ms), although following a delay (2-3 min). The decay to steady state of postextrasystolic potentiated beat was slower after endocardial damage than under control conditions. This suggested an increased Ca2+ recirculation through the sarcoplasmic reticulum between two consecutive beats (35% before Triton vs. 45% after Triton). Finally, in a medium containing 3 μM ryanodine, Triton treatment of the endocardial endothelium failed to induce any effect on either twitch force or action potential. Prolonged exposure to Triton X-100 (by a slow flow or high concentration) induced only deteriorating effects leading to substantial rise in the resting tension and generation of contractures and abbreviated action potentials with depressed plateau. These observations are consistent with the hypothesis that a modification in the sarcoplasmic reticulum function may, at least in part, be responsible for the observed changes in contractile function of the myocardium following endocardial damage with Triton treatment.en_US
dc.languageengen_US
dc.publisherN R C Research Press. The Journal's web site is located at http://pubs.nrc-cnrc.gc.ca/cgi-bin/rp/rp2_desc_e?cjppen_US
dc.relation.ispartofCanadian Journal of Physiology and Pharmacologyen_US
dc.subject.meshAction Potentials - Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCardiomyopathies - Physiopathologyen_US
dc.subject.meshCatsen_US
dc.subject.meshEndocardium - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHeart - Drug Effects - Physiology - Physiopathologyen_US
dc.subject.meshHeart Diseases - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Physiologyen_US
dc.subject.meshMyocardial Contraction - Drug Effects - Physiologyen_US
dc.subject.meshMyocardium - Cytologyen_US
dc.subject.meshOctoxynol - Pharmacologyen_US
dc.subject.meshPapillary Muscles - Drug Effects - Physiologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshRyanodine - Pharmacologyen_US
dc.subject.meshSystole - Physiologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVentricular Functionen_US
dc.titleModification of excitation-contraction coupling in cat ventricular myocardium following endocardial damageen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1139/y93-040-
dc.identifier.pmid8402389-
dc.identifier.scopuseid_2-s2.0-0027254255en_US
dc.identifier.volume71en_US
dc.identifier.issue3-4en_US
dc.identifier.spage254en_US
dc.identifier.epage262en_US
dc.identifier.isiWOS:A1993LN77500012-
dc.publisher.placeCanadaen_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridBanijamali, HS=6602222539en_US
dc.identifier.scopusauthoridChallice, CE=7004068919en_US

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