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Updated: Jun 23, 2026

Videomorphometric Analysis of Hypoxic Pulmonary Vasoconstriction of Intra-pulmonary Arteries Using Murine Precision Cut Lung Slices
Published on: January 14, 2014
Morphine is an arteriolar vasodilator in man
Reza Afshari1, Simon R J Maxwell, David J Webb
1Medical Toxicology Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran.
Intra-arterial morphine causes forearm vasodilatation via histamine and nitric oxide release, not opioid receptors. Further research is needed to explore opioid receptor mechanisms in arterial responses.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- The arterial effects of morphine are not fully understood.
- Investigating morphine's impact on vascular responses is crucial for clinical applications.
Purpose of the Study:
- To determine the forearm vascular responses to intra-arterial morphine in healthy subjects.
- To elucidate the mediating mechanisms of morphine-induced vasodilatation.
Main Methods:
- Forearm blood flow (FBF) was measured using venous occlusion plethysmography.
- Morphine was infused intra-arterially in a dose-ranging study, with assessments for acute tolerance.
- Mechanistic studies involved antagonists like naloxone, histamine receptor blockade, and nitric oxide (NO) clamp.
Main Results:
- Morphine significantly increased FBF in a dose-dependent manner.
- No acute tolerance to morphine's vasodilatory effect was observed.
- Vasodilatation was mediated by histamine and nitric oxide pathways, as it was blocked by antihistamines and NO clamp, but not by naloxone.
Conclusions:
- Intra-arterial morphine induces forearm vasodilatation.
- The vasodilatation is mediated by local histamine release and subsequent nitric oxide production.
- Opioid receptor involvement in these arterial effects requires further investigation.
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