›› 2010, Vol. 30 ›› Issue (3): 310-.

• Original article (Basic research) • Previous Articles     Next Articles

Effects of Hesperidin on cardiac electrophysiology of diabetic rats

WANG Wei1, CAO Jiu-mei1, YANG Zhi-fang2, WANG Hong-wei2, ZHANG Ying2, ZHAO Yong-ju1, LI Ci-zhen2   

  1. 1. Department of Geriatrics, Ruijing Hospital, School of Medicine, 2. Department of Physiology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2010-03-25 Published:2010-03-24
  • Supported by:

    Shanghai Education Committee Foundation, 05B212;Shanghai Science and Technology Committee Foundation, 06JC14045

Abstract:

Objective To investigate the effects of Hesperidin on cardiac electrophysiology of diabetic rats. Methods Thirty SD rats were randomly divided into three groups. Diabetic model group (n=12): diabetic model was induced by intraperitoneal injection of large amount of streptozotocin (STZ); Hesperidin intervention group (n=12): diabetic model was established, and were intragastrically administrated with 10 mg/kg Hesperidin daily; control group (n=6): without model establishment and intervention. After treatment for 4 weeks, in vivo and in vitro ECG and characteristics of action potentials of ventricular muscles were recorded and compared. Papillary muscles of ventricle of diabetic model group were perfused with 1×10-6 mol/L or 5×10-6 mol/L Hesperidin, and changes of action potentials were continuously recorded. Results In vivo ECG analysis revealed that the heart rates of diabetic model group and Hesperidin intervention group were much faster than that of control group (P<0.01, P<0.05), QT interval of diabetic model group significantly prolonged (P<0.05), while there was no significant difference in QT interval between control group and Hesperidin intervention group (P>0.05). In vitro ECG analysis indicated that the prevalence of tachyarrhythmia in diabetic model group was 75.0%, significantly higher than that of Hesperidin intervention group (16.7%)(P<0.05). Analysis of action potentials of ventricular muscles revealed that the resting membrane potential, amplitude of action potential and maximum upstroke velocity of phase 0 of diabetic model group were significantly lower than those of control group, while the action potential duration was longer than that of control group. Compared with diabetic model group, the parameters of action potentials in Hesperidin intervention group were more approximate with those of control group. Perfusion tests with two concentrations of Hesperidin demonstrated that 5×10-6 mol/L Hesperidin perfusion performed better than 1×10-6 mol/L Hesperidin perfusion in recovery of action potentials of papillary muscles of ventricle of diabetic rats. Conclusion Hesperidin may dose-dependently decrease the prevalence of arrhythmia by reversing the abnormal electrophysiological activities in diabetic rats.

Key words: diabetes mellitus, Hesperidin, cardiac electrophysiology, arrhythmia