• Our CiPA Instruments

    HESI FDA BAA study: "Assessing variability and reproducibility of manual and automated patch clamp platforms"

  • CiPA hERG Protocol

    This protocol was used for hERG studies on the Patchliner and SyncroPatch 384PE.

  • HTS CiPA hERG Assay

    Effects of Cisapride using the CiPA hERG protocol on the SyncroPatch 384PE

  • Myocyte & Ion Channel Effects

    Arrhythmic Field potentials in iPSC-derived Cardiomyocytes (CardioExcyte 96) and hERG current inhibition (SyncroPatch 384PE)

  • Gigaseal HTS patch clamp

    CiPA-specified cardiac ion channels recorded at high throughput

  • Gigaseal HTS patch clamp

    High throughput recordings of cardiac ion channels at physiological temperature

  • CardioExcyte 96 screening tool

    CardioExcyte 96 with integrated liquid handling for cardiac safety screening

hiPSC-CM - "Conduction velocity with the 2-electrode layout of the CardioExcyte 96"

Icon CE   CardioExcyte 96 Application Note   logo pdf   (1.4 MB)
Cardiosight®-S hiPSC-CMs kindly provided by Nexel


Cardiac conduction is the process by which electrical excitation spreads through the heart, triggering individual myocytes to contract synchronously. Slowed cardiac conduction velocity (CV) is associated with an increased risk of re-entrant excitation, leading to a pre-disposition to life-threatening arrhythmias1. 

CV is determined by the ion channel properties of cardiac myocytes and by their interconnections. It is strictly dependent on the maximum upstroke velocity of an action potential, which is determined by the sodium current2. In addition, gap junctions play a key role because they ultimately determine how much depolarizing sodium current passes from excited to non-excited regions of the network. Uncoupling of gap junctions causes discontinuities leading to slower CV. Defective intercellular coupling between the cardiomyocytes results in increased subthreshold depolarization, which slowly inactivates the voltage-gated sodium channels, further reducing the sodium current and excitability3.

In the case of collagenous scar tissue the uncoupling of myocyte–myocyte connections and subsequent coupling of myocytes with fibroblasts impairs the electrical conduction. In fact, collagen deposition results in electrically isolated fibers of viable myocardium, discontinuing the conduction path and globally reducing the action potential propagation velocity and consequently promoting the onset of re-entrant arrhythmias4. Since CV plays a pivotal role in cardiovascular diseases, it is essential to investigate the effect of a new compound on the cardiac CV.

In this study, we have investigated the effect of the sodium channel blocker lidocaine (30 and 100 μM) on CV in hiPSC-CMs (NEXEL Cardiosight®-S) using the CardioExcyte 96.

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