Electrophysiologic actions of pirmenol in dogs with recent myocardial infarction
dc.contributor.author | Lynch, Joseph J. | en_US |
dc.contributor.author | DiCarlo, Lorenzo A. | en_US |
dc.contributor.author | Montgomery, Daniel G. | en_US |
dc.contributor.author | Hassan, Terek | en_US |
dc.contributor.author | Lucchesi, Benedict Robert | en_US |
dc.date.accessioned | 2006-04-07T19:26:06Z | |
dc.date.available | 2006-04-07T19:26:06Z | |
dc.date.issued | 1986-10 | en_US |
dc.identifier.citation | Lynch, Joseph J., DiCarlo, Lorenzo A., Montgomery, Daniel G., Hassan, Terek, Lucchesi, Benedict R. (1986/10)."Electrophysiologic actions of pirmenol in dogs with recent myocardial infarction." American Heart Journal 112(4): 752-758. <http://hdl.handle.net/2027.42/26034> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6W9H-4BT895K-22/2/f7a65a6d7d421eaaca1f6de87c07fef9 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/26034 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3766375&dopt=citation | en_US |
dc.description.abstract | The electrophysiologic actions of pirmenol, an investigational class I antiarrhythmic agent, were evaluated in eight anesthetized dogs, 5 to 10 days after anterior myocardial infarction. Before administration of the drug, programmed ventricular stimulation failed to initiate nonsustained or sustained ventricular tachyarrhythmias (VT) in any of the postinfarction dogs. After the cumulative administration of 2.5, 5.0, and 10.0 mg/kg pirmenol, programmed stimulation initiated sustained VT in six of the eight postinfarction dogs tested, with one additional dog responding with reproducible nonsustained VT (15 to 20 monomorphic complexes) after pirmenol adminstration. Only one of eight postinfarction dogs tested remained noninducible throughout the primenol dosing schedule. Administration of pirmenol tended to increase ventricular excitation thresholds, relative (p p p < 0.01 after 2.5, 5, and 10, mg/kg) refractory periods between ischemically injured and normal noninjured ventricular myocardium. These findings suggest a potential for the provocation or aggravation of ventricular arrhythmias by pirmenol in the setting of recent myocardial infarction. | en_US |
dc.format.extent | 882970 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Electrophysiologic actions of pirmenol in dogs with recent myocardial infarction | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Mich., USA; Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, The University of Michigan Medical School, Ann Arbor, Mich., USA. | en_US |
dc.contributor.affiliationum | Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Mich., USA; Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA. | en_US |
dc.identifier.pmid | 3766375 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/26034/1/0000107.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0002-8703(86)90470-9 | en_US |
dc.identifier.source | American Heart Journal | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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