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Morphine-induced venodilation in humans

M Grossmann1, A Abiose, O Tangphao

  • 1Division of Clinical Pharmacology, Stanford University Medical Center, CA 94305-5113, USA.

Clinical Pharmacology and Therapeutics
|November 1, 1996
PubMed
Summary
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Morphine causes vasodilation in human hand veins, primarily through histamine release, not mu-opiate receptors. This finding clarifies the mechanism behind morphine

Area of Science:

  • Pharmacology
  • Vascular Biology
  • Pain Management

Background:

  • Morphine is used for pulmonary edema, potentially via peripheral venodilation.
  • The precise mechanism of opiate-induced venodilation in humans is not fully understood.

Purpose of the Study:

  • To investigate if opiates cause venodilation in human hand veins.
  • To explore the underlying mechanisms of opiate-mediated venodilation.

Main Methods:

  • Dorsal hand vein compliance technique in 15 healthy volunteers.
  • Dose-response curves for morphine and fentanyl after phenylephrine preconstriction.
  • Testing the effects of naloxone and histamine receptor antagonists on morphine's action.

Main Results:

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  • Morphine induced dose-dependent venodilation in human hand veins.
  • Fentanyl did not produce venodilation.
  • Histamine (H1 and H2) receptor antagonists completely blocked morphine's venodilatory effect, while naloxone had minimal impact.

Conclusions:

  • Morphine's venodilatory effect in human hand veins is mediated by histamine release.
  • Mu-opiate receptors play a minor role in this venodilatory response.