Document Detail


Rectification of the background potassium current: a determinant of rotor dynamics in ventricular fibrillation.
MedLine Citation:
PMID:  11739288     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ventricular fibrillation (VF) is the leading cause of sudden cardiac death. Yet, the mechanisms of VF remain elusive. Pixel-by-pixel spectral analysis of optical signals was carried out in video imaging experiments using a potentiometric dye in the Langendorff-perfused guinea pig heart. Dominant frequencies (peak with maximal power) were distributed throughout the ventricles in clearly demarcated domains. The fastest domain (25 to 32 Hz) was always on the anterior left ventricular (LV) wall and was shown to result from persistent rotor activity. Intermittent block and breakage of wavefronts at specific locations in the periphery of such rotors were responsible for the domain organization. Patch-clamping of ventricular myocytes from the LV and the right ventricle (RV) demonstrated an LV-to-RV drop in the amplitude of the outward component of the background rectifier current (I(B)). Computer simulations suggested that rotor stability in LV resulted from relatively small rectification of I(B) (presumably I(K1)), whereas instability, termination, and wavebreaks in RV were a consequence of strong rectification. This study provides new evidence in the isolated guinea pig heart that a persistent high-frequency rotor in the LV maintains VF, and that spatially distributed gradients in I(K1) density represent a robust ionic mechanism for rotor stabilization and wavefront fragmentation.
Authors:
F H Samie; O Berenfeld; J Anumonwo; S F Mironov; S Udassi; J Beaumont; S Taffet; A M Pertsov; J Jalife
Related Documents :
20348438 - Microvascular obstruction remains a portent of adverse remodeling in optimally treated ...
6496358 - Effect of successful thrombolytic therapy on right ventricular function in acute inferi...
19889228 - Predictors of right ventricular function as measured by tricuspid annular plane systoli...
1768348 - Using ultrasonic measurement of cardiac size in predicting congenital heart defect.
22940818 - Design and rationale of low-dose erythropoietin in patients with st-segment elevation m...
7457398 - Mexiletine for refractory-ventricular arrhythmias: results using serial electrophysiolo...
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation research     Volume:  89     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-12-12     Completed Date:  2002-01-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1216-23     Citation Subset:  IM    
Affiliation:
SUNY Upstate Medical University, Syracuse, NY, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Body Surface Potential Mapping
Computer Simulation
Electrocardiography
Electrophysiologic Techniques, Cardiac
Guinea Pigs
Heart Conduction System / physiopathology*
Heart Ventricles / pathology,  physiopathology*
Models, Cardiovascular
Patch-Clamp Techniques
Potassium / metabolism*
Potassium Channels, Inwardly Rectifying / metabolism*
Ventricular Fibrillation / etiology,  pathology,  physiopathology*
Grant Support
ID/Acronym/Agency:
1S10RR12917/RR/NCRR NIH HHS; HL60843/HL/NHLBI NIH HHS; P01 HL39707/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channels, Inwardly Rectifying; 7440-09-7/Potassium
Comments/Corrections
Comment In:
Circ Res. 2001 Dec 7;89(12):1089-91   [PMID:  11739272 ]

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


Previous Document:  Increased ischemia-induced angiogenesis in the staggerer mouse, a mutant of the nuclear receptor Ror...
Next Document:  Cytomegalovirus infection accelerates inflammation in vascular tissue overexpressing monocyte chemoa...