Effects of central sympathetic activation on repolarization-dispersion during short-term myocardial ischemia in anesthetized rats

• Published in: Life sciences (1973) 2016-01, Vol.144, p.170-177
• Main Authors: Kolettis, Theofilos M., La Rocca, Vassilios, Psychalakis, Nikolaos, Karampela, Eleftheria, Kontonika, Marianthi, Tourmousoglou, Christos, Baltogiannis, Giannis G., Papalois, Apostolos, Kyriakides, Zenon S.
• Format: Article
• Language: English
• Subjects: Anesthesia; Animals; Central sympathetic activation; Clonidine - pharmacology; Electrocardiography - drug effects; Heart Rate - drug effects; Ligation; Male; Myocardial ischemia; Myocardial Ischemia - physiopathology; Rats; Rats, Wistar; Repolarization-dispersion; Sympathetic Nervous System - physiopathology; Sympatholytics - pharmacology; Ventricular Function, Left - drug effects; Ventricular Function, Right - drug effects; Ventricular repolarization
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2015.12.019

Sympathetic activation during myocardial ischemia enhances arrhythmogenesis, but the underlying pathophysiologic mechanisms remain unclear. We investigated the central sympathetic effects on ventricular repolarization during the early-period post-coronary artery occlusion. We studied 12 Wistar rats (254±2g) for 30min following left coronary artery ligation, with (n=6) or without (n=6) pretreatment with the central sympatholytic agent clonidine. Mapping of left and right ventricular epicardial electrograms was performed with a 32-electrode array. As an index of sympathetic activation, heart rate variability in the frequency domain was calculated. Heart rate and repolarization duration were measured with a custom-made recording and analysis software, followed by calculation of intra- and inter-ventricular dispersion of repolarization. Heart rate and heart rate variability indicated lower sympathetic activation in clonidine-treated rats during ischemia. Repolarization duration in the left ventricle prolonged after clonidine at baseline, independently of heart rate, but no differences were present 30min post-ligation. Dispersion of repolarization in the right ventricle remained stable during ischemia, whereas it increased in the left ventricle, equally in both groups. A similar trend was observed for inter-ventricular dispersion, without differences between groups. In addition to intra-ventricular repolarization-dispersion, anterior-wall myocardial ischemia may also increase inter-ventricular repolarization-dispersion. Progressive central sympathetic activation occurs during myocardial ischemia, but it does not affect intra- or inter-ventricular dispersion of ventricular repolarization during the early phase. Further research is warranted on the potential effects during subsequent time-periods.