Ksenia Sedova1, Olesya Bernikova2, Jan Azarov3, Dmitry Shmakov2, Vladimir Vityazev2, Sergey Kharin4. 1. Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, 50, Pervomayskaya St, Syktyvkar, Russian Federation; Department of Biomedical Technology, Czech Technical University in Prague, Nam Sitna 3105, Kladno, Czech Republic. Electronic address: sedova.ks@gmail.com. 2. Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, 50, Pervomayskaya St, Syktyvkar, Russian Federation. 3. Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, 50, Pervomayskaya St, Syktyvkar, Russian Federation; Department of Physiology, Medical Institute of Syktyvkar State University, 11, Babushkin St, Syktyvkar, Russian Federation; Department of Physiology, Komi Branch of Kirov State Medical Academy, 11, Babushkin St, Syktyvkar, Russian Federation. 4. Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, 50, Pervomayskaya St, Syktyvkar, Russian Federation; Department of Physiology, Medical Institute of Syktyvkar State University, 11, Babushkin St, Syktyvkar, Russian Federation.
Abstract
BACKGROUND: Myocardial ischemic electrophysiological alterations are associated with the generation of reactive oxygen species. However, electrophysiological effects of antioxidants are unclear. Our objective was to determine the effects of the antioxidant echinochrome on ventricular repolarization in a feline model of 30-min ischemia. METHODS AND RESULTS: Activation-recovery intervals were measured from 64 ventricular electrograms recorded before and during the LAD ligation in untreated animals (controls, n=5) and animals given echinochrome (1mg/kg, n=5 and 2mg/kg, n=7). In controls, ischemia resulted in the increase of repolarization dispersion, QTc and Tpeak-Tend intervals and precordial T wave amplitude dispersion. Echinochrome attenuated the ischemic increase of repolarization dispersion. The increased dose of echinochrome abolished the ischemic ECG repolarization changes but did not modify the incidence of ventricular arrhythmias. CONCLUSION: Echinochrome modified ischemic alterations of repolarization dispersion that were associated with the changes of the body surface T wave amplitude dispersion and Tpeak-Tend interval.
BACKGROUND:Myocardial ischemic electrophysiological alterations are associated with the generation of reactive oxygen species. However, electrophysiological effects of antioxidants are unclear. Our objective was to determine the effects of the antioxidant echinochrome on ventricular repolarization in a feline model of 30-min ischemia. METHODS AND RESULTS: Activation-recovery intervals were measured from 64 ventricular electrograms recorded before and during the LAD ligation in untreated animals (controls, n=5) and animals given echinochrome (1mg/kg, n=5 and 2mg/kg, n=7). In controls, ischemia resulted in the increase of repolarization dispersion, QTc and Tpeak-Tend intervals and precordial T wave amplitude dispersion. Echinochrome attenuated the ischemic increase of repolarization dispersion. The increased dose of echinochrome abolished the ischemic ECG repolarization changes but did not modify the incidence of ventricular arrhythmias. CONCLUSION:Echinochrome modified ischemic alterations of repolarization dispersion that were associated with the changes of the body surface T wave amplitude dispersion and Tpeak-Tend interval.
Authors: Ksenia A Sedova; Olesya G Bernikova; Julia I Cuprova; Alexandra D Ivanova; Galina A Kutaeva; Michael G Pliss; Ekaterina V Lopatina; Marina A Vaykshnorayte; Emiliano R Diez; Jan E Azarov Journal: Int J Mol Sci Date: 2019-12-15 Impact factor: 5.923