Document Detail

Role of KATP channel in electrical depression and asystole during long-duration ventricular fibrillation in ex vivo canine heart.
MedLine Citation:
PMID:  22467302     Owner:  NLM     Status:  MEDLINE    
Long-duration ventricular fibrillation (LDVF) in the globally ischemic heart is characterized by transmurally heterogeneous decline in ventricular fibrillation rate (VFR), emergence of inexcitable regions, and eventual global asystole. Rapid loss of both local and global excitability is detrimental to successful defibrillation and resuscitation during cardiac arrest. We sought to assess the role of the ATP-sensitive potassium current (I(KATP)) in the timing and spatial pattern of electrical depression during LDVF in a structurally normal canine heart. We analyzed endo-, mid-, and epicardial unipolar electrograms and epicardial optical recordings in the left ventricle of isolated canine hearts during 10 min of LDVF in the absence (control) and presence of an I(KATP) blocker glybenclamide (60 μM). In all myocardial layers, average VFR was the same or higher in glybenclamide-treated than in control hearts. The difference increased with time of LDVF and was overall significant in all layers (P < 0.05). However, glybenclamide did not significantly affect the transmural VFR gradient. In epicardial optical recordings, glybenclamide shortened diastolic intervals, prolonged action potential duration, and decreased the percentage of inexcitable area (all differences P < 0.001). During 10 min of LDVF, asystole occurred in 55.6% of control and none of glybenclamide-treated hearts (P < 0.05). In three hearts paced after the onset of asystole, there was no response to LV epicardial or atrial pacing. In structurally normal canine hearts, I(KATP) opening during LDVF is a major factor in the onset of local and global inexcitability, whereas it has a limited role in overall deceleration of VFR and the transmural VFR gradient.
Tyson G Taylor; Paul W Venable; Junko Shibayama; Mark Warren; Alexey V Zaitsev
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-03-30
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  302     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-06-04     Completed Date:  2012-09-12     Revised Date:  2014-10-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2396-409     Citation Subset:  IM    
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MeSH Terms
Glyburide / pharmacology
Heart Arrest / physiopathology*
KATP Channels / antagonists & inhibitors,  drug effects,  physiology*
Models, Animal
Time Factors
Ventricular Fibrillation / physiopathology*
Voltage-Sensitive Dye Imaging
Grant Support
1F32-HL-097576/HL/NHLBI NIH HHS; 1R01-HL-103877/HL/NHLBI NIH HHS; 5R01-HL-088444/HL/NHLBI NIH HHS; R01 HL088444/HL/NHLBI NIH HHS
Reg. No./Substance:
0/KATP Channels; SX6K58TVWC/Glyburide

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

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