The involvement of gap junctions in the delayed phase of the protection induced by cardiac pacing in dogs

Márton Gönczi, Mária Kovács, György Seprényi, A. Végh

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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 C×43 (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 ischaemiainduced structural impairment of the intercalated discs, and preserved GJ permeability and C×43 phosphorylation, without modifying C×43 protein content. Following cardiac pacing the membrane and total C×43 protein contents were unchanged up to 6 h, but were significantly reduced 12 h later (preceded by a down-regulation of C×43 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 C×43 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.

Original languageEnglish
Pages (from-to)39-51
Number of pages13
JournalClinical Science
Volume123
Issue number1
DOIs
Publication statusPublished - Jul 2012

Fingerprint

Connexin 43
Gap Junctions
Dogs
Cardiac Arrhythmias
Reperfusion
Ischemia
Ventricular Premature Complexes
Anti-Arrhythmia Agents
Electric Impedance
Permeability
Coronary Vessels
Proteins
Down-Regulation
Phosphorylation
Messenger RNA
Membranes

Keywords

  • Arrhythmia
  • Cardiac pacing
  • Connexin43
  • Delayed protection
  • Gap junction
  • Ischaemia/reperfusion

ASJC Scopus subject areas

  • Medicine(all)

Cite this

The involvement of gap junctions in the delayed phase of the protection induced by cardiac pacing in dogs. / Gönczi, Márton; Kovács, Mária; Seprényi, György; Végh, A.

In: Clinical Science, Vol. 123, No. 1, 07.2012, p. 39-51.

Research output: Contribution to journalArticle

Gönczi, Márton ; Kovács, Mária ; Seprényi, György ; Végh, A. / The involvement of gap junctions in the delayed phase of the protection induced by cardiac pacing in dogs. In: Clinical Science. 2012 ; Vol. 123, No. 1. pp. 39-51.
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