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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

[Transient change of cardiac action potential and intracellular Ca2+ during ventricular fibrillation]

Su-hua Wu1, Hideki Hayashi, Shien-fong Lin

  • 1Department of Cardiology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China.

Zhonghua Xin Xue Guan Bing Za Zhi
|December 23, 2008
PubMed

Insights

The coupling between cardiac action potential (AP) and intracellular calcium transient (CaT) remains strong during rapid heart rates, but dissociates during ventricular fibrillation (VF), independent of activation rate.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Electrophysiology
  • Calcium Signaling

Context:

  • The cardiac action potential (AP) and intracellular calcium transient (CaT) are tightly coupled under normal conditions.
  • This association is disrupted during ventricular fibrillation (VF), a life-threatening arrhythmia.
  • The underlying cause for this dissociation, particularly concerning the high activation rates during VF, remains unclear.

Purpose:

  • To investigate whether the dissociation between AP and CaT during VF is directly related to the high ventricular activation rate.
  • To quantify the coupling between AP and CaT under various rapid pacing conditions and during VF.

Summary:

  • Simultaneous optical mapping of AP and CaT was performed in isolated rabbit hearts.
  • Pinacidil, a K(ATP) channel opener, was used to induce rapid pacing and ventricular tachycardia (VT) comparable to VF rates.
  • Mutual information (MI) analysis revealed that AP-CaT coupling was significantly higher during fast pacing and fast VT compared to VF, irrespective of the activation rate.

Impact:

  • Demonstrates that the dissociation between AP and CaT during VF is not solely a consequence of rapid activation.
  • Suggests that other factors intrinsic to VF contribute to the disruption of normal electro-calcium coupling.
  • Provides insights into the mechanisms underlying arrhythmogenesis and potential targets for antiarrhythmic therapies.
Abstract

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