Document Detail

Adaptation to high altitude hypoxia protects the rat heart against ischemia-induced arrhythmias. Involvement of mitochondrial K(ATP) channel.
MedLine Citation:
PMID:  10525420     Owner:  NLM     Status:  MEDLINE    
The aim was to determine whether adaptation to chronic hypoxia protects the heart against ischemic arrhythmias and whether ATP-dependent potassium channels (K(ATP)) play a role in the antiarrhythmic mechanism. Adult male rats were adapted to intermittent high altitude hypoxia (5000 m, 4 h/day) and susceptibility to ischemia-induced ventricular arrhythmias was evaluated in the Langendorff-perfused hearts subjected to either an occlusion of the coronary artery for 30 min or pre-conditioning by brief occlusion of the same artery prior to 30-min reocclusion. In separate groups, either a K(ATP) blocker, glibenclamide (10 micromol/l), or a mitochondrial K(ATP) opener, diazoxide (50 micromol/l), were added to a perfusion medium 20 min before the occlusion. Adaptation to hypoxia reduced the total number of ventricular arrhythmias by 64% as compared with normoxic controls. Preconditioning by a single 3-min coronary artery occlusion was antiarrhythmic only in the normoxic group, while two occlusion periods of 5 min each were needed to pre-condition the hypoxic hearts. Glibenclamide increased the number of arrhythmias in the normoxic hearts from 1316+/-215 to 2091+/-187 (by 59%) and in the hypoxic group from 636+/-103 to 1777+/-186 (by 179%). In contrast, diazoxide decreased the number of arrhythmias only in the normoxic group from 1374+/-96 to 582+/-149 (by 58%), while its effect in the hypoxic group was not significant. It is concluded that long-term adaptation of rats to high altitude hypoxia decreases the susceptibility of their hearts to ischemic arrhythmias and increases an antiarrhythmic threshold of pre-conditioning. The mitochondrial K(ATP) channel, rather than the sarcolemmal K(ATP) channel, appears to be involved in the protective mechanism afforded by adaptation.
G Asemu; F Papousek; B Ostádal; F Kolár
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  31     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1999 Oct 
Date Detail:
Created Date:  1999-11-05     Completed Date:  1999-11-05     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:  1821-31     Citation Subset:  IM; S    
Copyright Information:
Copyright 1999 Academic Press.
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
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MeSH Terms
Arrhythmias, Cardiac / etiology,  physiopathology,  prevention & control*
Glyburide / pharmacology
Heart / physiology*,  physiopathology
Heart Rate / drug effects
Heart Ventricles
Ion Channels / physiology
Membrane Proteins / physiology*
Mitochondria, Heart / physiology*
Myocardial Ischemia / physiopathology*
Potassium Channels
Rats, Wistar
Reg. No./Substance:
0/Ion Channels; 0/Membrane Proteins; 0/Potassium Channels; 0/mitochondrial K(ATP) channel; 10238-21-8/Glyburide

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