Document Detail


Intracellular calcium and the mechanism of anodal supernormal excitability in langendorff perfused rabbit ventricles.
MedLine Citation:
PMID:  21301131     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Anodal stimulation hyperpolarizes the cell membrane and increases the intracellular Ca(2+) (Ca(i)) transient. This study tested the hypothesis that the maximum slope of the Ca(i) decline (-(dCa(i)/dt)(max)) corresponds to the timing of anodal dip on the strength-interval curve and the initiation of repetitive responses and ventricular fibrillation (VF) after a premature stimulus (S(2)).
METHODS AND RESULTS: We simultaneously mapped the membrane potential (V(m)) and Ca(i) in 23 rabbit ventricles. A dip in the anodal strength-interval curve was observed. During the anodal dip, ventricles were captured by anodal break excitation directly under the S(2) electrode. The Ca(i) following anodal stimuli is larger than that following cathodal stimuli. The S(1)-S(2) intervals of the anodal dip (203±10 ms) coincided with the -(dCa(i)/dt)(max) (199±10 ms, P=NS). BAPTA-AM (n=3), inhibition of the electrogenic Na(+)-Ca(2+) exchanger current (I(NCX)) by low extracellular Na(+) (n=3), and combined ryanodine and thapsigargin infusion (n=2) eliminated the anodal supernormality. Strong S(2) during the relative refractory period (n=5) induced 29 repetitive responses and 10 VF episodes. The interval between S(2) and the first non-driven beat was coincidental with the time of -(dCa(i)/dt)(max).
CONCLUSIONS: Larger Ca(i) transient and I(NCX) activation induced by anodal stimulation produces anodal supernormality. The time of maximum I(NCX) activation is coincidental to the induction of non-driven beats from the Ca(i) sinkhole after a strong premature stimulation.
Authors:
Boyoung Joung; Hyung-Wook Park; Mitsunori Maruyama; Liang Tang; Juan Song; Seongwook Han; Gianfranco Piccirillo; James N Weiss; Shien-Fong Lin; Peng-Sheng Chen
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-02-02
Journal Detail:
Title:  Circulation journal : official journal of the Japanese Circulation Society     Volume:  75     ISSN:  1347-4820     ISO Abbreviation:  Circ. J.     Publication Date:  2011  
Date Detail:
Created Date:  2011-03-28     Completed Date:  2011-08-12     Revised Date:  2013-03-11    
Medline Journal Info:
Nlm Unique ID:  101137683     Medline TA:  Circ J     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  834-43     Citation Subset:  IM    
Copyright Information:
All rights are reserved to the Japanese Circulation Society.
Affiliation:
Krannert Institute of Cardiology and the Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism*
Electric Stimulation / methods
Electrodes
Heart Ventricles / metabolism*
Membrane Potentials*
Perfusion
Rabbits
Grant Support
ID/Acronym/Agency:
P01 HL078931/HL/NHLBI NIH HHS; P01 HL78931/HL/NHLBI NIH HHS; R01 HL071140/HL/NHLBI NIH HHS; R01 HL078932/HL/NHLBI NIH HHS; R01 HL71140/HL/NHLBI NIH HHS; R01 HL78932/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
7440-70-2/Calcium
Comments/Corrections

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