The present study has examined the role of GJ (gap junctions) in the delayed anti-arrhythmic effect of cardiac pacing, with particular reference to the time-course changes in Cx43 (connexin43) expression both after pacing (4×5 min, at a rate of 240 beats/min) and 24 h later, when the dogs were subjected to a 25 min occlusion and reperfusion of the LAD (left anterior descending coronary artery). Compared with the SP (sham-paced) controls (n=20), in dogs paced 24 h previously (n=16) there were reductions in arrhythmia severity [e.g. number of VPB (ventricular premature beats) during occlusion 294±78 compared with 63±25; survival from the combined ischaemia/reperfusion insult 20% compared with 78%], and in other ischaemic changes [epicardial ST-segment, TAT (total activation time) and tissue impedance]. Pacing also prevented the ischaemia-induced structural impairment of the intercalated discs, and preserved GJ permeability and Cx43 phosphorylation, without modifying Cx43 protein content. Following cardiac pacing the membrane and total Cx43 protein contents were unchanged up to 6 h, but were significantly reduced 12 h later (preceded by a down-regulation of Cx43 mRNA at 6 h), and returned to normal by 24 h. Interestingly, dogs that were subjected to ischaemia 12 h after cardiac pacing showed increased arrhythmia generation. We conclude that cardiac pacing results in time-dependent changes in Cx43 expression, which may alter GJ function and influence arrhythmia generation during a subsequent ischaemia/reperfusion insult. This effect is manifested in protection 24 h after pacing, but of potential clinical interest is the finding that there is a time interval after pacing during which an ischaemic event may generate severe ventricular arrhythmias.
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Research Article|
March 12 2012
The involvement of gap junctions in the delayed phase of the protection induced by cardiac pacing in dogs
Márton Gönczi;
Márton Gönczi
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary
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Mária Kovács;
Mária Kovács
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary
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György Seprényi;
György Seprényi
†Department of Medical Biology, University of Szeged, Szeged, Hungary
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Ágnes Végh
*Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary
Correspondence: Professor Ágnes Végh (email [email protected]).
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Publisher: Portland Press Ltd
Received:
September 30 2011
Revision Received:
January 06 2012
Accepted:
January 16 2012
Accepted Manuscript online:
January 16 2012
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2012 Biochemical Society
2012
Clin Sci (Lond) (2012) 123 (1): 39–51.
Article history
Received:
September 30 2011
Revision Received:
January 06 2012
Accepted:
January 16 2012
Accepted Manuscript online:
January 16 2012
Citation
Márton Gönczi, Mária Kovács, György Seprényi, Ágnes Végh; The involvement of gap junctions in the delayed phase of the protection induced by cardiac pacing in dogs. Clin Sci (Lond) 1 July 2012; 123 (1): 39–51. doi: https://doi.org/10.1042/CS20110501
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