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Related Experiment Videos

Arrhythmias caused by platelet activating factor

B F Hoffman1, S D Guo, S J Feinmark

  • 1Department of Pharmacology, Columbia University, New York, New York 10032, USA.

Journal of Cardiovascular Electrophysiology
|February 1, 1996
PubMed
Summary
This summary is machine-generated.

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Platelet-activating factor (PAF) causes dangerous heart rhythm changes in ventricular myocytes. This finding suggests PAF released by neutrophils during reperfusion may trigger arrhythmias in heart attack patients.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Electrophysiology
  • Pharmacology

Background:

  • Ischemia and reperfusion are linked to ventricular arrhythmias.
  • Neutrophils infiltrate ischemic areas, activating and releasing platelet-activating factor (PAF).
  • The role of PAF in cardiac myocyte arrhythmogenesis requires investigation.

Purpose of the Study:

  • To investigate the arrhythmogenic effects of platelet-activating factor (PAF) on canine cardiac myocyte transmembrane potentials.
  • To determine the dose-dependent actions of PAF on myocyte electrophysiology.
  • To explore the potential role of PAF in reperfusion-induced arrhythmias.

Main Methods:

  • Canine cardiac myocytes were isolated and studied in vitro.
  • Transmembrane potentials were recorded under control conditions and during superfusion with graded doses of PAF.

Related Experiment Videos

  • PAF receptor antagonist (CV-6209) and ion channel blockers (tetrodotoxin, xylocaine) were used to assess mechanisms.

    • Main Results:

    • PAF induced dose-dependent increases in action potential duration and early afterdepolarizations (EADs).
    • Transient arrest of repolarization (PA) and small depolarizations were observed with PAF exposure.
    • PAF's arrhythmogenic effects were transient and antagonized by CV-6209, tetrodotoxin, and xylocaine.

    Conclusions:

    • Platelet-activating factor (PAF) exerts consistent arrhythmogenic effects on ventricular myocyte membranes.
    • PAF released by activated neutrophils during reperfusion is a significant factor in arrhythmias.
    • This mechanism may also contribute to arrhythmias during myocardial infarction evolution.