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Related Experiment Videos

Morphine attenuates leukocyte/endothelial interactions.

X Ni1, K R Gritman, T K Eisenstein

  • 1Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania, 19140, USA.

Microvascular Research
|August 31, 2000
PubMed
Summary

Morphine use may reduce immune cell sticking during sepsis, potentially by increasing nitric oxide (NO) production. This effect was blocked by naloxone and a specific NO inhibitor, suggesting a role for NO in morphine

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Area of Science:

  • Immunology
  • Pharmacology
  • Microcirculation Research

Background:

  • Gram-negative sepsis and endotoxic shock post-surgery are significant global health issues.
  • Morphine, a common postoperative pain reliever, is suspected to impair immune function and increase sepsis risk.
  • Understanding morphine's impact on leukocyte behavior is crucial for managing postoperative complications.

Purpose of the Study:

  • To investigate whether morphine attenuates leukocyte rolling and sticking in microcirculation.
  • To determine if this effect is mediated by nitric oxide (NO) production.
  • To explore the role of opioid receptors in morphine's effects on leukocyte-endothelial interactions.

Main Methods:

  • Utilized a dorsal skinfold chamber model in nude mice for intravital fluorescence microscopy.

Related Experiment Videos

  • Administered slow-release morphine pellets and evaluated leukocyte/endothelial interactions after oxidized low-density lipoprotein injection.
  • Investigated the role of nitric oxide synthase (NOS) inhibition using NG-nitro-l-arginine (NOLA) and aminoguanidine (AG).

    • Main Results:

    • Morphine significantly reduced leukocyte rolling and sticking in both arterioles and venules.
    • Naloxone pellets reversed the attenuating effects of morphine.
    • NO synthase inhibition with NOLA, but not AG, reversed the morphine-induced attenuation.

    Conclusions:

    • Morphine interferes with leukocyte/endothelial cell interactions.
    • This interference appears to be mediated through the stimulation of nitric oxide production.
    • The findings suggest a potential mechanism by which morphine might influence inflammatory responses in sepsis.