Document Detail


Ionic mechanisms of the depression of automaticity and conduction in the rabbit atrioventricular node caused by hypoxia or metabolic inhibition and protective action of glucose and valine.
MedLine Citation:
PMID:  2480705     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effects of hypoxia and a metabolic inhibitor, sodium cyanide (NaCN), on the spontaneous action potential and membrane current systems were studied in small preparations (0.2 x 0.2 x 0.1 mm) of rabbit atrioventricular node. When the PO2 of the superfusate was lowered from 500 to less than 20 mm Hg, all the preparations initially showed reductions in the spontaneous firing frequency (due to the decreased rate of diastolic depolarization) and maximal rate of depolarization, which were followed by a cessation of automatic activity with subsequent membrane hyperpolarization to -57 +/- 3 mV (n = 4). Voltage clamp experiments using double microelectrode techniques revealed that hypoxia reduced the slow inward current by 20 to 80% without affecting its inactivation kinetics. The delayed rectifying potassium current tail was also reduced or abolished by severe hypoxia, whereas the background outward current was greatly increased. The hyperpolarization-activated inward current was decreased by hypoxia. Similar changes in the spontaneous action potential and membrane currents were obtained on adding 0.1 to 0.5 mM NaCN to the superfusate under conditions of normal PO2. Hypoxia-induced suppression of automaticity was reversed completely by 5 mM glucose, and partially by 40 mM valine. These results suggest that (1) hypoxia impairs atrioventricular nodal conduction by reducing the slow inward current and the delayed rectifying potassium current; (2) hypoxia depresses automaticity by increasing the background outward current and, to some extent, by reducing the slow inward current; and (3) glucose and valine contribute to the generation of high-energy phosphates in cytoplasm and mitochondria, respectively, and protect the atrioventricular node from hypoxia.
Authors:
M Nishimura; H Tanaka; N Homma; T Matsuzawa; Y Watanabe
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of cardiology     Volume:  64     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  1989 Dec 
Date Detail:
Created Date:  1990-01-17     Completed Date:  1990-01-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  24J-28J     Citation Subset:  AIM; IM    
Affiliation:
Cardiovascular Institute, Fujita Gakuen Health University School of Medicine, Aichi, Japan.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / drug effects
Animals
Anoxia / physiopathology*
Atrioventricular Node / physiopathology*
Biomechanics
Female
Glucose / pharmacology*
Heart Conduction System / physiopathology*
Ion Channels / physiology
Ions
Leucine / pharmacology
Male
Myocardium / metabolism*
Neural Conduction
Rabbits
Sodium Cyanide / pharmacology
Valine / pharmacology*
Chemical
Reg. No./Substance:
0/Ion Channels; 0/Ions; 143-33-9/Sodium Cyanide; 50-99-7/Glucose; 61-90-5/Leucine; 7004-03-7/Valine

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


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