| Reversibility of electrophysiologic abnormalities of subendocardial Purkinje fibers induced by ischemia. | |
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MedLine Citation:
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PMID: 8055146 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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INTRODUCTION: During the subacute phase of infarction in the canine heart, the subendocardial Purkinje fibers subtended by the infarct show depolarization greater than can be accounted for by the decrease in [K+]i, and generate abnormal action potentials and spontaneous rhythms due to abnormal automaticity. We have used pinacidil to hyperpolarize these fibers and evaluate the extent to which an increase in resting potential can normalize action potential generation. METHODS AND RESULTS: Twenty-four hours after two-stage ligation of the canine left anterior descending coronary artery, preparations of subendocardial Purkinje fibers were studied in vitro by recording transmembrane potentials through standard microelectrodes and exposing the preparation to pinacidil and increases in [K+]o. Pinacidil increased resting potential to the estimated value of EK, abolished the abnormal automaticity, and restored action potentials of normal amplitude with normal values of Vmax. This effect often persisted after washout of pinacidil. Elevation of [K+]o from 4.0 to 20.0 mM slightly increased maximum diastolic potential, suggesting that the excess (over the change in EK) depolarization was caused by a decrease in gK1. CONCLUSION: The ventricular arrhythmias seen during the subacute stage of infarction probably are caused by abnormal automaticity. Our findings support the conclusion that this abnormal automaticity arises in partially depolarized subendocardial Purkinje fibers. This loss of resting potential is due in large part to a decrease in gK1. Restoration of resting potential to the value of EK permits the Purkinje fibers to develop essentially normal action potentials. An agent capable of reversing the partial block of IK,1 thus might be an effective drug for some types of arrhythmias. |
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Authors:
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X L Ren; B F Hoffman |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of cardiovascular electrophysiology Volume: 5 ISSN: 1045-3873 ISO Abbreviation: J. Cardiovasc. Electrophysiol. Publication Date: 1994 May |
Date Detail:
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Created Date: 1994-09-13 Completed Date: 1994-09-13 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9010756 Medline TA: J Cardiovasc Electrophysiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 412-21 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Columbia University, College of Physicians and Surgeons, New York, New York 10032. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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physiology Animals Diastole Dogs Electrophysiology Endocardium / physiopathology* Female Guanidines / pharmacology Male Membrane Potentials / drug effects Myocardial Infarction / physiopathology Myocardial Ischemia / physiopathology* Osmolar Concentration Pinacidil Potassium / metabolism Potassium Channels / metabolism Purkinje Fibers / physiopathology* |
| Grant Support | |
ID/Acronym/Agency:
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HL-08508/HL/NHLBI NIH HHS; HL-30557/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Guanidines; 0/Potassium Channels; 56-65-5/Adenosine Triphosphate; 7440-09-7/Potassium; 85371-64-8/Pinacidil |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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