Document Detail


Proposed role of energy supply in the genesis of delayed afterdepolarizations--implications for ischemic or reperfusion arrhythmias.
MedLine Citation:
PMID:  2448488     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Delayed afterdepolarizations (DADs) are Ca++-dependent electrophysiological abnormalities, which are evoked by a variety of conditions that induce intracellular Ca++ overload, including fast pacing, isoproterenol, dibutyryl cyclic AMP, and intracellular injection of Ca++. Since Ca++ overload is suspected of playing a role in both ischemic and reperfusion cellular damage, a reasonable hypothesis would be that DADs could play a role in ischemic or reperfusion arrhythmias. No direct proof has, however, been obtained for such a role for DADs. We propose that DADs could be associated with arrhythmias in which there is Ca++ overload of sufficient magnitude to cause an increased oscillatory release of Ca++ from the sarcoplasmic reticulum (SR), provided energy is available in the form of ATP. A sustained increase of Ca++ is likely to reflect energy depletion and therefore exclude a significant contribution of DADs to arrhythmia development. Thus, DADs are more likely to play a role in: (i) reperfusion arrhythmias and (ii) arrhythmias arising in moderately ischemic tissue, than in severe ischemia with marked energy depletion.
Authors:
W A Coetzee; L H Opie; S Saman
Related Documents :
12717098 - Na+/h+ exchange inhibition with cardioplegia reduces cytosolic [ca2+] and myocardial da...
3366798 - In vivo fluorometric measurement of changes in cytosolic free calcium from the cat cort...
1718698 - Basic mechanisms involved in the protection of the ischaemic myocardium. the role of ca...
15592578 - Sea0400: a novel sodium-calcium exchange inhibitor with cardioprotective properties.
9056088 - Intracellular calcium increase in gerbil taste cell by amino acid sweeteners.
23318498 - Intracellular renin alters the electrical properties of the intact heart ventricle of a...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  19 Suppl 5     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1987 Oct 
Date Detail:
Created Date:  1988-03-15     Completed Date:  1988-03-15     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  13-21     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Cape Town, Observatory, South Africa.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Arrhythmias, Cardiac / etiology*,  metabolism
Calcium / metabolism*
Coronary Circulation*
Coronary Disease / complications*
Energy Metabolism
Guinea Pigs
Heart Conduction System / physiopathology
Ion Channels / metabolism*
Myocardial Contraction
Papillary Muscles / physiology
Chemical
Reg. No./Substance:
0/Ion Channels; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Effects of lidocaine on single cardiac sodium channels.
Next Document:  Adenine nucleotides and ventricular fibrillation.