Isoproterenol-induced heart failure in rats caused significant changes in ventricular repolarization and increased repolarization heterogeneity, independent of myocardial hypertrophy.
Does isoproterenol-induced heart failure alter ventricular repolarization in female Wistar rats?
Isoproterenol-induced heart failure in rats causes significant changes in ventricular repolarization and increased repolarization heterogeneity, independent of myocardial hypertrophy.
Isoproterenol in high doses induces infarction-like myocardial damage and structural and functional remodelling of the ventricular myocardium. The purpose of the present study was to investigate ventricular repolarization in a rat model of isoproterenol-induced heart failure. Isoproterenol was administered twice to female Wistar rats (170 mg/kg, s.c., 24 h apart). Four weeks after the injections, cardiac output was measured and unipolar epicardial ventricular electrograms were recorded in situ. Activation-recovery intervals were calculated to assess repolarization. Histological examination of the heart ventricles was also performed. Heart failure in rats treated with isoproterenol was indicated by myocardial histopathological damage and reduced cardiac output. In rats with heart failure, the regional differences in activation-recovery interval prolongation over the ventricular epicardium resulted in increasing heterogeneity in the activation-recovery interval distribution and increasing repolarization heterogeneity of the ventricular subepicardium. Myocardial damage and haemodynamic changes in heart failure induced by isoproterenol were accompanied by significant changes in ventricular repolarization, which were not associated with myocardial hypertrophy.
Krandycheva et al. (Sat,) conducted a other in Heart failure. Isoproterenol was evaluated on Ventricular repolarization (activation-recovery intervals). Isoproterenol-induced heart failure in rats caused significant changes in ventricular repolarization and increased repolarization heterogeneity, independent of myocardial hypertrophy.
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