Further evidence for the role of gap junctions in the delayed antiarrhythmic effect of cardiac pacing
The objective of this study was to provide evidence that gap junctions are involved in the delayed antiarrhythmic effect of cardiac pacing. Twenty-four dogs were paced through the right ventricle (4 × 5 min, rate of 240 beats/min) 24 h prior to a 25 min occlusion of the left anterior descending coronary artery. Some of these paced dogs were infused with 50 (n = 7) or 100 μmol/L (n = 7) of the gap junction uncoupler carbenoxolone (CBX), prior to and during the occlusion. Ten sham-paced dogs, subjected only to occlusion, served as the controls. Cardiac pacing markedly reduced the number of ectopic beats and episodes of ventricular tachycardia (VT), as well the incidence of VT and ventricular fibrillation during occlusion. The changes in severity of ischaemia and tissue electrical resistance were also less marked compared with the unpaced controls. Pacing also preserved the permeability of gap junctions, the phosphorylation of connexin43, and the structural integrity of the intercalated discs. The closing of gap junctions with CBX prior to and during ischaemia markedly attenuated or even abolished these protective effects of pacing. Conclusion: Our results support the previous findings that gap junctions play a role in the delayed antiarrhythmic effect of cardiac pacing.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
Document Type: Research Article
Publication date: January 1, 2015
More about this publication?
- Published since 1929, this monthly journal reports new research in the fields of physiology and pharmacology.
- Editorial Board
- Information for Authors
- Submit a Paper
- Subscribe to this Title
- Sign up for journal newsletters
- Ingenta Connect is not responsible for the content or availability of external websites