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Related Experiment Videos

Systemically administered alpha2-agonist-induced peripheral vasoconstriction in humans.

Pekka Talke1, Errol Lobo, Ronald Brown

  • 1Department of Anesthesia and Perioperative Medicine, University of California, San Francisco, 94143, USA. talkep@anesthesia.ucsf.edu

Anesthesiology
|June 27, 2003
PubMed
Summary

Dexmedetomidine causes vasoconstriction by activating alpha(2)-adrenoceptors. This study isolated vasoconstrictive effects by reducing sympatholytic activity, revealing dose-dependent vasoconstriction in sympathectomized hands.

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Area of Science:

  • Pharmacology
  • Cardiovascular Physiology

Background:

  • Alpha(2)-adrenoceptors influence both sympatholytic and vasoconstrictive effects.
  • Selective alpha(2)-adrenoceptor agonists can have dual hemodynamic actions.

Purpose of the Study:

  • To isolate and characterize the peripheral vasoconstrictive effects of dexmedetomidine.
  • To understand vasoconstriction independent of sympatholytic actions.

Main Methods:

  • Administered increasing concentrations of dexmedetomidine or placebo to volunteers.
  • Attenuated sympatholytic effects via general anesthesia or brachial plexus block.
  • Measured finger blood volume (vasoconstriction) and hemodynamics.

Main Results:

  • Anesthetized volunteers showed vasoconstriction (increased LTF) with dexmedetomidine.

Related Experiment Videos

  • Awake volunteers exhibited vasodilation (decreased LTF) in neurally intact hands.
  • Dexmedetomidine induced dose-dependent vasoconstriction in sympathectomized hands.
  • Conclusions:

    • First characterization of the lower dose-response curve for dexmedetomidine-induced vasoconstriction.
    • Sympathetic nervous system activity significantly modulates alpha(2)-agonist vasoconstrictive effects.
    • Dexmedetomidine's vasoconstrictive potential can be observed by minimizing sympatholysis.