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PMID: 2421289 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

Bacaner MB, Clay JR, Shrier A, Brochu RM

Abstract

The suppression of ventricular fibrillation by antidysrhythmic drugs is well correlated with their ability to block potassium channels in nerve and cardiac membranes. Blockade of potassium channels reduces electrical inhomogeneities in action potential and conduction parameters that lead to ventricular fibrillation. These actions tend to effectively decrease the electrical size of the heart, which suggests a mechanism for antifibrillatory drug action. The receptor sites for antifibrillatory drug action (IK blockade) appear to be on the outside of the cardiac membrane whereas receptors for antiarrhythmic drug action (INa blockade) appear to be on the inside of the cardiac membrane.

MeSH Terms
4-Aminopyridine Aminopyridines/pharmacology Animals Bethanidine/pharmacology Bretylium Compounds/pharmacology Cesium/pharmacology Chickens Decapodiformes Dogs Guanethidine/pharmacology Ion Channels/physiology Lidocaine/pharmacology Methylguanidine/analogs & derivatives,pharmacology Procainamide/pharmacology Tetraethylammonium Compounds/pharmacology Ventricular Fibrillation/chemically induced,physiopathology
Chemicals
Aminopyridines Bretylium Compounds Ion Channels Tetraethylammonium Compounds Cesium Methylguanidine Lidocaine 4-Aminopyridine Procainamide bretylium meobentine Bethanidine Guanethidine
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Bacaner M B
Clay J R
Shrier A
Brochu R M
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51 references, click to expand
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
Published
1986-04-00
Pages
2223-7
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC323264
Subset
IM
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