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Acute microcirculatory effects of platelet-activating factor.

W N Durán1, P K Dillon

  • 1Department of Physiology, UMDNJ-New Jersey Medical School, Newark 07103-2757.

Journal of Lipid Mediators
|January 1, 1990
PubMed
Summary

Platelet-activating factor (PAF) affects microcirculation by increasing macromolecule leakage and leukocyte adhesion in a dose-dependent manner. Its effects on permeability involve leukotrienes, while vasoconstriction is mediated by thromboxane.

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Area of Science:

  • Microcirculation research
  • Inflammatory mediator studies

Background:

  • Platelet-activating factor (PAF) is a potent inflammatory mediator.
  • Understanding PAF's role in microvascular responses is crucial for inflammatory disease research.

Purpose of the Study:

  • To quantify the dose-response effects of topically applied PAF on microvascular permeability, vessel diameter, and leukocyte adhesion.
  • To investigate the biochemical pathways mediating PAF's actions.

Main Methods:

  • Hamster cheek pouch preparation.
  • Intravital microscopy and fluorometry.
  • Assessment of macromolecular clearance and leukocyte adhesion.
  • Use of arachidonic acid cascade inhibitors and receptor blockers.

Main Results:

  • PAF increased macromolecular clearance dose-dependently (max at 10(-7) M).
  • Maximal vasoconstriction occurred at 10(-5) M PAF.
  • PAF (10(-9) M) induced leukocyte adhesion without altering vessel diameter or permeability.
  • Dexamethasone and kadsurenone attenuated clearance; indometacin and OKY-046 prevented vasoconstriction.

Conclusions:

  • PAF induces dose-related macromolecular extravasation, potentially via leukotrienes.
  • PAF-induced vasoconstriction is thromboxane-mediated.
  • PAF stimulates leukocyte adhesion inversely with dose.
  • PAF responses are partially receptor-mediated.

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