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Article: Effect of lidoflazine on systemic arteries and veins

TitleEffect of lidoflazine on systemic arteries and veins
Authors
Issue Date1980
PublisherSage Publications, Inc. The Journal's web site is located at http://ang.sagepub.com
Citation
Angiology, 1980, v. 31 n. 9, p. 581-593 How to Cite?
AbstractLidoflazine, 4 4,4-bis(4 fluorophenyl)butyl-N-(2,6dimethylphenyl)-1-piperazineacetamide, helps improve work tolerance in patients with ischemic heart disease. Chronic treatment with the drug in patients with angina pectoris increase stroke volume, decreases systemic vascular resistance, and reduces mean arterial pressure at rest. Similar results were described in intact animals on acute administration of the compound. In both normal volunteers and patients with ischemic heart disease, chronic administration of lidoflazine augments stroke volume and cardiac output, and decreases mean arterial pressure and systemic vascular resistance during exercise. These hemodynamic findings indicate that the myocardium is shifted from pressure work to volume work, and that its total load (preload and afterload) is reduced by lidoflazine. The major dynamic determinants of preload and afterload of the heart are the degree of constriction of the venous and arterial segments of the circulation, respectively. This study was designed to determine the direct effects of lidoflazine on arterial and venous smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/170616
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 0.695
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorVerbeuren, TJen_US
dc.contributor.authorVan Nueten, JMen_US
dc.date.accessioned2012-10-30T06:10:09Z-
dc.date.available2012-10-30T06:10:09Z-
dc.date.issued1980en_US
dc.identifier.citationAngiology, 1980, v. 31 n. 9, p. 581-593en_US
dc.identifier.issn0003-3197en_US
dc.identifier.urihttp://hdl.handle.net/10722/170616-
dc.description.abstractLidoflazine, 4 4,4-bis(4 fluorophenyl)butyl-N-(2,6dimethylphenyl)-1-piperazineacetamide, helps improve work tolerance in patients with ischemic heart disease. Chronic treatment with the drug in patients with angina pectoris increase stroke volume, decreases systemic vascular resistance, and reduces mean arterial pressure at rest. Similar results were described in intact animals on acute administration of the compound. In both normal volunteers and patients with ischemic heart disease, chronic administration of lidoflazine augments stroke volume and cardiac output, and decreases mean arterial pressure and systemic vascular resistance during exercise. These hemodynamic findings indicate that the myocardium is shifted from pressure work to volume work, and that its total load (preload and afterload) is reduced by lidoflazine. The major dynamic determinants of preload and afterload of the heart are the degree of constriction of the venous and arterial segments of the circulation, respectively. This study was designed to determine the direct effects of lidoflazine on arterial and venous smooth muscle.en_US
dc.languageengen_US
dc.publisherSage Publications, Inc. The Journal's web site is located at http://ang.sagepub.comen_US
dc.relation.ispartofAngiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Drug Effectsen_US
dc.subject.meshCocaineen_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshLidoflazine - Pharmacologyen_US
dc.subject.meshNorepinephrine - Metabolismen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPiperazines - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshSaphenous Vein - Metabolismen_US
dc.subject.meshTibiaen_US
dc.subject.meshVeins - Drug Effectsen_US
dc.titleEffect of lidoflazine on systemic arteries and veinsen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1177/000331978003100901-
dc.identifier.pmid7212379-
dc.identifier.scopuseid_2-s2.0-0019191960en_US
dc.identifier.volume31en_US
dc.identifier.issue9en_US
dc.identifier.spage581en_US
dc.identifier.epage593en_US
dc.identifier.isiWOS:A1980KR50200001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridVerbeuren, TJ=7007006534en_US
dc.identifier.scopusauthoridVan Nueten, JM=7005700327en_US
dc.identifier.issnl0003-3197-

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