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Related Experiment Video

Updated: Jul 9, 2026

Contractions of Human-iPSC-derived Cardiomyocyte Syncytia Measured with a Ca-sensitive Fluorescent Dye in Temperature-controlled 384-well Plates
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Endotoxin impairs the human pacemaker current If.

Klaus Zorn-Pauly1, Brigitte Pelzmann, Petra Lang

  • 1Institut für Biophysik, Zentrum für Physiologische Medizin, Medizinische Universität Graz, Harrachgasse 21, Graz, Austria.

Shock (Augusta, Ga.)
|December 20, 2007
PubMed
Summary
This summary is machine-generated.

Lipopolysaccharides (LPSs) impair the heart's pacemaker current (I(f)), potentially explaining reduced heart rate variability in sepsis. This finding highlights LPS's direct impact on cardiac function.

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10:53

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Published on: July 3, 2013

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pathophysiology

Background:

  • Sepsis, often triggered by gram-negative bacteria, involves lipopolysaccharides (LPSs) that affect host cells, including ionic channels.
  • Reduced heart rate variability is a known clinical manifestation of human sepsis and endotoxemia.

Purpose of the Study:

  • To investigate the hypothesis that LPS directly affects the pacemaker current (I(f)) in the human heart.
  • To determine if LPS-induced alterations in I(f) contribute to the reduced heart rate variability observed in sepsis.

Main Methods:

  • Isolated human atrial myocytes were incubated with LPS (1 and 10 microg/mL) for 6-10 hours.
  • The pacemaker current (I(f)) was measured using the whole-cell patch-clamp technique at 37°C.
  • A spontaneously active sinoatrial cell model was used for simulations.

Main Results:

  • Incubation with 10 microg/mL LPS significantly impaired I(f) by suppressing current at potentials positive to -80 mV and slowing activation, without altering maximal conductance.
  • The response of I(f) to beta-adrenergic stimulation (isoproterenol) was significantly larger in LPS-treated cells.
  • Simulations showed that LPS-induced I(f) impairment reduced the model cell's responsiveness to autonomic input.

Conclusions:

  • Lipopolysaccharides (LPSs) have a direct detrimental impact on the cardiac pacemaker current (I(f)) in human atrial myocytes.
  • LPS-induced I(f) impairment may be a key factor contributing to reduced heart rate variability in septic conditions.
  • These findings are relevant to understanding cardiac dysfunction in sepsis and other conditions where endotoxin plays a role, such as heart failure.