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Related Experiment Videos

Action potentials that mimic fibrillation activate sodium current.

M R Ujhelyi1, T L Creazzo

  • 1University of Georgia College of Pharmacy, Augusta, GA, USA. michael.ujhelyi@medtronic.com

Journal of Molecular and Cellular Cardiology
|September 2, 1999
PubMed
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Sodium channels remain active during ventricular fibrillation (VF), even with very short rest periods. This sodium current contributes to action potential propagation during VF, challenging previous assumptions.

Area of Science:

  • Cardiovascular Physiology
  • Ion Channel Electrophysiology
  • Cardiac Arrhythmias

Background:

  • Ventricular fibrillation (VF) is characterized by extremely brief action potentials and diastolic intervals.
  • Under these conditions, the role of sodium channels in action potential generation and propagation is uncertain.
  • Previous research suggested sodium channel activation might be compromised during VF due to short diastolic intervals.

Purpose of the Study:

  • To investigate whether sodium channels can be activated during simulated ventricular fibrillation conditions.
  • To quantify the fast inward sodium current under conditions mimicking VF.
  • To determine the impact of short action potential durations and diastolic intervals on sodium channel function.

Main Methods:

  • Isolated chick ventricular myocytes were voltage-clamped to measure sodium current.

Related Experiment Videos

  • A voltage-clamp protocol simulated VF using a 10-pulse train at 10 Hz with varying depolarization intervals (90-20 ms).
  • Test pulses were applied after each train to assess sodium current activation, inactivation, and recovery.

    • Main Results:

    • Sodium current was detectable during brief resting intervals as short as 20 ms.
    • Short resting intervals (<60 ms) shifted the sodium conductance activation curve to more depolarized potentials.
    • Less sodium channel inactivation and faster recovery from inactivation were observed with shorter prepulses, facilitating sodium current during simulated VF.

    Conclusions:

    • Inward sodium current is evident even with diastolic rest intervals as short as 10-20 ms.
    • Sodium channel activation, inactivation, and recovery are influenced by the interplay of rest interval, depolarization length, and membrane potential.
    • These findings suggest that sodium channels contribute to wavefront propagation during ventricular fibrillation by maintaining inward sodium current despite brief action potentials and short diastolic intervals.