| Effect of E4031, a class III antiarrhythmic drug, on ischemia- and reperfusion-induced arrhythmias in isolated rat hearts. | |
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MedLine Citation:
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PMID: 9687827 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The delayed outward rectifier K+ channel has a role in the increase in automaticity of myocytes under pathophysiological conditions. The purpose of the present study was to clarify the effect of blockade of outward rectifier K+ channels by a class III antiarrhythmic drug, E4031, on ischemia- and reperfusion-induced arrhythmias. Ion fluxes, energy metabolites and cardiac function were measured and the epicardial electrocardiograms of Langendorff-perfused rat hearts were recorded during initial perfusion, global or regional ischemia and reperfusion. 10(-7) M of E4031 administered during the initial perfusion did not prolong the QT interval, but slowed the heart rate (Control: 222, E4031: 183 bpm, p < 0.05), increased myocardial 45Ca2+ uptake (Control: 2.1, E4031: 2.9 mumol/g dwt, p < 0.05) and attenuated the loss of intracellular K+ during ischemia (Control: 238, E4031: 248 mumol/g dwt, p < 0.05). E4031 tended to reduce ischemia-induced ventricular tachyarrhythmias (Control: 60, E4031: 30%, n.s.), but reperfusion-induced ventricular tachyarrhythmias were sustained longer by the administration of E4031 (Control: 255, E4031: 623 sec, p < 0.05). Prior exposure to E4031 decreased the depletion of high energy phosphates during ischemia, but suppressed their recovery during reperfusion. These results suggest that the attenuated loss of K+ from the ischemic myocardium and the decrease in heart rate by E4031 contributed to the reduction of ischemia-induced arrhythmias. However, the increase in myocardial Ca2+ uptake and altered energy metabolism may be responsible for the increase in reperfusion-induced arrhythmias. |
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Authors:
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K Shinmura; M Tani; H Hasegawa; Y Ebihara; Y Nakamura |
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Publication Detail:
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Type: In Vitro; Journal Article |
Journal Detail:
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Title: Japanese heart journal Volume: 39 ISSN: 0021-4868 ISO Abbreviation: Jpn Heart J Publication Date: 1998 Mar |
Date Detail:
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Created Date: 1998-08-18 Completed Date: 1998-08-18 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0401175 Medline TA: Jpn Heart J Country: JAPAN |
Other Details:
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Languages: eng Pagination: 183-97 Citation Subset: IM |
Affiliation:
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Department of Geriatric Medicine, Keio University School of Medicine, Tokyo, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Arrhythmia Agents / pharmacology, therapeutic use* Arrhythmias, Cardiac / drug therapy*, physiopathology Calcium / metabolism Energy Metabolism / drug effects Heart / drug effects* Male Myocardial Reperfusion Injury / drug therapy*, physiopathology Myocardium / metabolism Piperidines / pharmacology, therapeutic use* Potassium Channels / drug effects Pyridines / pharmacology, therapeutic use* Rats Rats, Sprague-Dawley Ventricular Function, Left / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Anti-Arrhythmia Agents; 0/Piperidines; 0/Potassium Channels; 0/Pyridines; 113558-89-7/E 4031; 7440-70-2/Calcium |
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