Transmembrane action potentials and the electrocardiogram in rats with renal hypertension
The results of previous studies of the relation between the surface electrocardiogram and cellular transmembrane potentials have suggested that the T wave configuration of the ECG is the result of a difference in the duration of endocardial and epicardial action potentials. Ventricular hypertrophy i...
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Published in | Cardiovascular research Vol. 15; no. 11; pp. 611 - 614 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
01.11.1981
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Subjects | |
Online Access | Get full text |
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Summary: | The results of previous studies of the relation between the surface electrocardiogram and cellular transmembrane potentials have suggested that the T wave configuration of the ECG is the result of a difference in the duration of endocardial and epicardial action potentials. Ventricular hypertrophy induced by renal hypertension in rats is associated with lengthening of action potential duration and a reproducible decrease in T wave magnitude. Therefore, this model was used to study the relation between the surface T wave configuration and regional differences in action potential duration. ECGs were recorded from hypertensive (HBP) and sham-operated (SHAM) rats. The hearts from these animals were removed and transmembrane action potentials were recorded by standard microelectrode techniques from endocardial and epicardial preparations. We found that the normally peaked T waves seen in the ECG of SHAM rats was reduced by 35% in the ECG of HBP rats. This reduction of T wave magnitude was associated with similar duration of epicardial and endocardial action potentials in HBP rats. However, peaked T wave in SHAM ECG was not accompanied by a significant disparity in the duration of the epicardial and endocardial action potentials. Thus, there is no simple, consistent correlation between surface T wave configuration and regional differences in intracellular action potential duration in rats. |
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Bibliography: | ArticleID:15-11-611 ark:/67375/HXZ-TMH86SDJ-V Address for correspondece and reprint requests: Ronald S Aronson, MD, Division of Cardiology, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA. istex:6DEDC1C48E78E51C2BC7A6D86F357D95ACE26836 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0008-6363 1755-3245 |
DOI: | 10.1093/cvr/15.11.611 |