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33rd International Congress on Electrocardiology

International Society of Electrocardiology

Effects Of Insulin On Triggered Activity In Hamster Ventricular Myocytes

Meeting Abstract

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  • corresponding author presenting/speaker C.-I. Lin - Institute Physiology, Natl Def Med Ctr, Taipei, Taiwan
  • C.-H. Hsu - Institute Med Sci, Natl Def Med Ctr, Taipei, Taiwan
  • Y.-C. Chen - Dept Biomed Engin, Natl Def Med Ctr, Taipei, Taiwan
  • J. Wei - Cheng-Hsin Gen Hosp, Taipei, Taiwan

33rd International Congress on Electrocardiology. Cologne, 28.06.-01.07.2006. Düsseldorf, Köln: German Medical Science; 2007. Doc06ice058

The electronic version of this article is the complete one and can be found online at:

Published: February 8, 2007

© 2007 Lin et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Question: The mechanisms of triggered arrhythmias in heart failure likely involve triggered activity from either delayed afterdepolarizations (DADs) or early afterdeoplarizations (EADs). Because insulin would increase the [Ca2+]i in failing heart, it might result in Ca2+ overload and induce cardiac arrhythmias. In animal models as well as in clinical trials, insulin had been shown to prevent ventricular arrhythmias and atrial fibrillation. The aim of the present study was to clarify the arrhythmogenic and antiarrhythmic effects of insulin on healthy and dilated myopathic (Bio 14.6) Syrian hamster ventricular myocytes (male, 33-41 week-old).

Methods used: Enzymes were used to isolate myocytes. Transient inward current (Iti) was elicited at clamped potential from –40 to +40 mV for different durations ranging from 50 to 3050 ms and then repolarized to –40 mV and/or repolarization after trains of depolarizing pulses (from -40 to +40 mV for 500 ms in duration) for 20 times.

Results: Exposure to insulin (1 µM) increased the amplitude of steady-state outward IK on depolarization but reduced markedly the magnitude of Iti on repolarization. Similar results were obtained in 16 hamster ventricular myocytes. However, in 3 of 19 myocytes tested, insulin increased Iti on repolarization, which could be reversed by an inhibitor of Na+-Ca2+ exchanger (NCX). Insulin also tended to shorten AP duration and decrease the incidence of EADs. The actions of insulin were partially reversible after washout.

Conclusion: Arrhythmogenic or antiarrhythmic effects of insulin varied from one hamster ventricular myocyte to another. Effects of insulin on triggered activity depended on individual electrophysiological properties such as ICa,L, INCX and outward K+ currents (Ito and IK).