Morphine modulates inducible nitric oxide synthase expression and reduces pulmonary oedema induced by

Mustafa Comert1, Emine Yilmaz Sipahi, Huseyin Ustun

  • 1Department of General Surgery, Faculty of Medicine, Zonguldak Karaelmas University, Zonguldak, Turkey.

Insights

Morphine prevents lung injury caused by alpha-naphthylthiourea (ANTU) by acting on peripheral opioid receptors. This protective effect against ANTU-induced pulmonary edema and inflammation was dose-dependent and blocked by naloxone.

Area of Science:

  • Pharmacology
  • Toxicology
  • Pulmonary Medicine

Background:

  • Alpha-naphthylthiourea (ANTU) is a chemical agent known to induce pulmonary edema.
  • The precise mechanisms underlying ANTU-induced lung injury are not fully understood.

Purpose of the Study:

  • To investigate the role of morphine in preventing alpha-naphthylthiourea (ANTU)-induced pulmonary edema.
  • To explore the involvement of peripheral opioid receptors in this protective effect.

Main Methods:

  • Rats were injected with ANTU to induce pulmonary edema.
  • Morphine was administered prior to ANTU, and its effects were assessed.
  • Naloxone methiodide, an opioid receptor antagonist, was used to investigate the mechanism.
  • Inducible nitric oxide synthase (iNOS) expression was examined using immunohistochemistry.

Main Results:

  • ANTU injection significantly increased lung weight/body weight ratio and caused pleural effusion.
  • Pre-treatment with morphine dose-dependently inhibited ANTU-induced pulmonary edema.
  • The protective effect of morphine was reversed by naloxone methiodide.
  • Morphine administration reduced the expression of inducible nitric oxide synthase (iNOS) in ANTU-treated rats.

Conclusions:

  • Subcutaneous morphine exhibits a preventive effect against ANTU-induced pulmonary inflammation and edema.
  • This protective action is mediated through peripheral opioid receptors.
  • Endogenous opioids do not appear to play a significant role in modulating ANTU-induced lung damage.

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