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Intrathecally injected morphine inhibits inflammatory paw edema: the involvement of nitric oxide and cyclic-guanosine monophosphate.
Anesth Analg. 2008 Mar; 106(3):965-71, table of contents.A&A

Abstract

BACKGROUND

Morphine can inhibit inflammatory edema in experimental animals. The mechanisms and sites by which opioids exert this effect are still under debate. Since the spinal level is a site for modulation of the neurogenic component of inflammation, we investigated the effect of intrathecal (i.t.) administration of morphine, and the involvement of spinal nitric oxide (NO)/cyclic-guanosine monophosphate-GMP pathway in carrageenan (CG)-induced paw edema.

METHODS

Male Wistar rats received i.t. injections of drugs (20 microL) 30 min before paw stimulation with CG (150 microg). Edema was measured as paw volume increase (mL), and neutrophil migration was evaluated indirectly by myeloperoxidase (MPO) assay.

RESULTS

Morphine (37, 75, and 150 nmol) inhibited inflammatory edema, but had no effect on MPO activity. Coinjection with naloxone (64 nmol) reversed the effect of morphine. The corticosteroid synthesis inhibitor, aminoglutethimide (50 mg/kg, v.o.), administered 90 min before morphine injection did not modify its antiedematogenic effect. Low doses of the NO synthase inhibitor, N(omega)-nitro-L-arginine (L-NNA; 10 and 30 pmol) increased, while higher doses (3 and 30 nmol) inhibited edema. The guanylate cyclase inhibitor 1H-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 21 and 42 nmol) increased, while the phosphodiesterase type 5 inhibitor sildenafil (0.15 and 1.5 nmol) inhibited paw edema. Coadministration of a subeffective dose of L-NNA (3 pmol) or ODQ (10 nmol) with morphine prevented its antiedematogenic effect, but sildenafil (0.15 nmol) rendered a subeffective dose of morphine effective (18 nmol). ODQ also prevented the antiedematogenic effect of the NO donor S-nitroso-N-acetyl-penicilamine.

CONCLUSION

These results support the idea that morphine can act on opioid receptors at the spinal level to produce antiedematogenic, and that the NO/cGMP pathway seems to be an important mediator in this effect.

Authors+Show Affiliations

Departamento de Farmacologia, CCB, Universidade Federal de Santa Catarina, Florianópolis, SC, 88040-900, Brasil.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18292447

Citation

Brock, Sara Comelli, and Carlos Rogério Tonussi. "Intrathecally Injected Morphine Inhibits Inflammatory Paw Edema: the Involvement of Nitric Oxide and Cyclic-guanosine Monophosphate." Anesthesia and Analgesia, vol. 106, no. 3, 2008, 965-71, table of contents.
Brock SC, Tonussi CR. Intrathecally injected morphine inhibits inflammatory paw edema: the involvement of nitric oxide and cyclic-guanosine monophosphate. Anesth Analg. 2008;106(3):965-71, table of contents.
Brock, S. C., & Tonussi, C. R. (2008). Intrathecally injected morphine inhibits inflammatory paw edema: the involvement of nitric oxide and cyclic-guanosine monophosphate. Anesthesia and Analgesia, 106(3), 965-71, table of contents. https://doi.org/10.1213/ane.0b013e318162cebf
Brock SC, Tonussi CR. Intrathecally Injected Morphine Inhibits Inflammatory Paw Edema: the Involvement of Nitric Oxide and Cyclic-guanosine Monophosphate. Anesth Analg. 2008;106(3):965-71, table of contents. PubMed PMID: 18292447.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intrathecally injected morphine inhibits inflammatory paw edema: the involvement of nitric oxide and cyclic-guanosine monophosphate. AU - Brock,Sara Comelli, AU - Tonussi,Carlos Rogério, PY - 2008/2/23/pubmed PY - 2008/3/12/medline PY - 2008/2/23/entrez SP - 965-71, table of contents JF - Anesthesia and analgesia JO - Anesth Analg VL - 106 IS - 3 N2 - BACKGROUND: Morphine can inhibit inflammatory edema in experimental animals. The mechanisms and sites by which opioids exert this effect are still under debate. Since the spinal level is a site for modulation of the neurogenic component of inflammation, we investigated the effect of intrathecal (i.t.) administration of morphine, and the involvement of spinal nitric oxide (NO)/cyclic-guanosine monophosphate-GMP pathway in carrageenan (CG)-induced paw edema. METHODS: Male Wistar rats received i.t. injections of drugs (20 microL) 30 min before paw stimulation with CG (150 microg). Edema was measured as paw volume increase (mL), and neutrophil migration was evaluated indirectly by myeloperoxidase (MPO) assay. RESULTS: Morphine (37, 75, and 150 nmol) inhibited inflammatory edema, but had no effect on MPO activity. Coinjection with naloxone (64 nmol) reversed the effect of morphine. The corticosteroid synthesis inhibitor, aminoglutethimide (50 mg/kg, v.o.), administered 90 min before morphine injection did not modify its antiedematogenic effect. Low doses of the NO synthase inhibitor, N(omega)-nitro-L-arginine (L-NNA; 10 and 30 pmol) increased, while higher doses (3 and 30 nmol) inhibited edema. The guanylate cyclase inhibitor 1H-oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 21 and 42 nmol) increased, while the phosphodiesterase type 5 inhibitor sildenafil (0.15 and 1.5 nmol) inhibited paw edema. Coadministration of a subeffective dose of L-NNA (3 pmol) or ODQ (10 nmol) with morphine prevented its antiedematogenic effect, but sildenafil (0.15 nmol) rendered a subeffective dose of morphine effective (18 nmol). ODQ also prevented the antiedematogenic effect of the NO donor S-nitroso-N-acetyl-penicilamine. CONCLUSION: These results support the idea that morphine can act on opioid receptors at the spinal level to produce antiedematogenic, and that the NO/cGMP pathway seems to be an important mediator in this effect. SN - 1526-7598 UR - https://www.unboundmedicine.com/medline/citation/18292447/Intrathecally_injected_morphine_inhibits_inflammatory_paw_edema:_the_involvement_of_nitric_oxide_and_cyclic_guanosine_monophosphate_ L2 - https://doi.org/10.1213/ane.0b013e318162cebf DB - PRIME DP - Unbound Medicine ER -