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Electrophysiologic effects of interactions between activated canine neutrophils and cardiac myocytes

B F Hoffman1, S J Feinmark, S D Guo

  • 1Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.

Journal of Cardiovascular Electrophysiology
|June 1, 1997
PubMed

Insights

Activated neutrophils bound to cardiac myocytes generate platelet-activating factor (PAF), causing arrhythmias. Blocking PAF receptors prevents these arrhythmogenic effects, suggesting PAF

Area of Science:

  • Cardiovascular Physiology
  • Immunology
  • Cardiac Electrophysiology

Background:

  • Myocardial ischemia leads to neutrophil binding on myocytes, releasing platelet-activating factor (PAF).
  • PAF is known to induce delayed repolarization, early afterdepolarizations (EADs), and repolarization arrest.
  • The study investigates if activated neutrophils on myocytes generate PAF and affect cardiac electrical activity.

Purpose of the Study:

  • To determine if activated neutrophils bound to canine cardiac myocytes generate PAF.
  • To investigate if this neutrophil activation causes changes in myocyte transmembrane potentials similar to PAF.
  • To assess the role of PAF receptor blockade in mitigating these effects.

Main Methods:

  • Canine cardiac myocytes and neutrophils were superfused, and transmembrane potentials were recorded.
  • Neutrophils were added to myocytes and activated using zymosan-activated serum (ZAS).
  • Platelet-activating factor (PAF) generation was quantified, and PAF receptor blockade was employed using CV-6209.

Main Results:

  • Activated neutrophils induced action potential prolongation, EADs, and plateau arrest in myocytes.
  • These electrophysiological changes mimicked those caused by exogenous PAF.
  • Significant PAF liberation was detected from activated neutrophils, and PAF receptor blockade prevented the observed electrical alterations.

Conclusions:

  • Activation of neutrophils bound to cardiac myocytes causes arrhythmogenic changes in myocyte electrical activity.
  • These effects are mediated by PAF generation and are preventable by PAF receptor blockade.
  • Platelet-activating factor (PAF) generated by activated neutrophils is a likely contributor to arrhythmias during myocardial reperfusion.
Abstract

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