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Morphine‐induced venodilation in humans
Author(s) -
Grossmann Matthias,
Abiose Ademola,
Tangphao Oranee,
Blaschke Terrence F.,
Hoffman Brian B.
Publication year - 1996
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/s0009-9236(96)90151-4
Subject(s) - morphine , medicine , (+) naloxone , opiate , pharmacology , agonist , fentanyl , phenylephrine , opioid receptor , anesthesia , opioid , receptor , blood pressure
Morphine has been extensively used in the treatment of pulmonary edema, and its action is believed to be mediated in part by its ability to produce peripheral venodilation. This study investigated whether opiates produce venodilation in human hand veins and explored the underlying mechanism(s). Fifteen healthy volunteers (11 men and four women) were studied with use of the dorsal hand vein compliance technique. After preconstriction with the selective α 1 ‐adrenergic receptor agonist phenylephrine, dose‐response curves were constructed to (1) opiate receptor agonists morphine (1 to 30 μg/min) or fentanyl (0.07 to 1 μg/min), (2) a combination of morphine and the μ‐opiate receptor antagonist naloxone, and (3) morphine and a combination of histamine (H 1 and H 2 ) receptor antagonists. Infusion of morphine caused venodilation in a dose‐dependent manner, whereas fentanyl did not produce venodilation. Coinfusion of naloxone and morphine impaired the venodilation only slightly. Coinfusion of the H 1 ‐ and H 2 ‐antagonists completely abolished the venodilatory effect of morphine. These results suggest that the venodilatory effect of morphine is mediated through histamine release and that μ‐opiate receptors have little or no involvement in this process. Clinical Pharmacology & Therapeutics (1996) 60 , 554–560; doi: