Abstract
We investigated whether morphine and fentanyl influence surface receptor expression, phagocytic activity and superoxide anion generation of neutrophils in a whole blood flow cytometric assay. Morphine suppressed complement and Fcgamma receptor expression and neutrophil function in a concentration- and time-dependent manner. Morphine-induced changes were similar to those caused by the nitric oxide (NO) donor S-nitroso-N-acetyl-penicillamine and were abolished by preincubation with the NO synthase inhibitor N-nitro-L-arginine as well as naloxone. Fentanyl had no immunosuppressive effects. These results suggest that these neutrophil functions are inhibited by morphine-stimulated NO release mediated by the mu(3) opiate receptor subtype found on immunocytes.
MeSH terms
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Fentanyl / pharmacology
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Flow Cytometry
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Humans
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In Vitro Techniques
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Male
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Morphine / pharmacology*
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Naloxone / pharmacology
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Narcotic Antagonists / pharmacology
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Narcotics / pharmacology*
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Neutrophils / chemistry
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Neutrophils / drug effects
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Neutrophils / metabolism*
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Nitric Oxide / metabolism*
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Nitric Oxide Donors / pharmacology
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Penicillamine / analogs & derivatives*
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Penicillamine / pharmacology
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Phagocytosis / drug effects
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Phagocytosis / immunology
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Receptors, Complement / biosynthesis*
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Receptors, Complement / immunology
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Receptors, IgG / metabolism
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Receptors, Opioid, mu / metabolism*
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Respiratory Burst / drug effects
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Respiratory Burst / immunology
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S-Nitroso-N-Acetylpenicillamine
Substances
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Narcotic Antagonists
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Narcotics
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Nitric Oxide Donors
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Receptors, Complement
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Receptors, IgG
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Receptors, Opioid, mu
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Nitric Oxide
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Naloxone
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Morphine
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S-Nitroso-N-Acetylpenicillamine
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Penicillamine
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Fentanyl