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Specific opiate effects on dextran-induced inflammation in rats.
M G Zeitune1, E Bazerque, P M Bazerque
1Cátedra de Farmacología, Facultad de Odontología, UBA, Argentina.
Acta Physiologica, Pharmacologica Et Therapeutica Latinoamericana : Organo De La Asociacion Latinoamericana De Ciencias Fisiologicas Y [De] La Asociacion Latinoamericana De Farmacologia
|January 1, 1991
Summary
Opiates like morphine modulate acute inflammation in rats by reducing paw edema and enhancing vascular permeability. Naltrexone, an opiate antagonist, blocks these morphine effects, indicating a specific role for opiates in inflammatory responses.
Area of Science:
- Pharmacology
- Inflammation Research
- Neuroscience
Background:
- Acute inflammation is a complex biological response.
- Opiates are known for their analgesic properties, but their role in inflammation is less understood.
Purpose of the Study:
- To investigate the effects of opiates on acute inflammatory models in rats.
- To determine the specific modulatory role of opiates in inflammatory responses.
Main Methods:
- Two models of acute inflammation were induced in rats using dextran solution.
- Morphine (0.1-10 mg/kg, i.p.) and naltrexone (10 mg/kg, i.p.) were administered.
- Paw edema and skin vascular permeability were measured.
- Lidocaine was used for local anesthesia to rule out its involvement.
Main Results:
- Morphine significantly inhibited dextran-induced paw edema by 50%.
- Low doses of naltrexone also inhibited edema, while high doses did not.
- Naltrexone (10 mg/kg) completely blocked the anti-edema effect of morphine.
- Morphine enhanced skin vascular permeability by 50%, an effect also prevented by naltrexone.
- Lidocaine did not affect edema or morphine's inhibitory effects.
Conclusions:
- Opiates play a specific modulatory role in acute inflammatory responses in rats.
- The observed effects of morphine on inflammation are mediated through opiate receptors, as evidenced by naltrexone's antagonism.
- These findings suggest potential therapeutic implications for opiate-based modulation of inflammation.