The role of rat brain mast cell histamine in the analgesic effect of morphine, and the possible involvement of cyclooxygenase products of arachidonic acid, was studied in the tail-flick and hot-plate tests. In animals submitted to repeated anphylactoid reactions (by injecting compound 48/80 intracerebroventricularly, 20 μg/5 μl, for five days) morphine (10 mg/kg, sc, 24 hrs after the last treatment with compound 48/80) showed a significant enhancement in its antinociceptive properties and a marked increase in the duration of action in both analgesic tests, compared to saline-pretreated rats. In rats pretreated with combined compound 48/80 (20 μg, icv) plus the nonsteroidal antiinflammatory drug acetylsalicyclic acid (30 mg/kg, ip. 60 min before compound 48/80) for five days, the effect of morphine (10 mg/kg, sc, 24 hrs after) was reduced both in its intensity and in its duration of analgesic efficacy, compared to saline-pretreated rats. Since in this study acetylsalicylic acid-pretreatment was shown to inhibit the morphine response in tailflick and hot-plate tests only in animals lacking in brain mast cell histamine following icv administration of compound 48/80, results suggest that cyclooxygenase products of arachidonic acid may be intermediates in the adaptive processes involved in shock/stress functional disturbances in rat brain. © 1993 Birkhäuser Verlag.

Increased analgesic potency of morphine following repeated anaphylactoid reaction by compound 48/80 involves cyclooxygenase products of arachidonic acid

Chiechio S.;
1993-01-01

Abstract

The role of rat brain mast cell histamine in the analgesic effect of morphine, and the possible involvement of cyclooxygenase products of arachidonic acid, was studied in the tail-flick and hot-plate tests. In animals submitted to repeated anphylactoid reactions (by injecting compound 48/80 intracerebroventricularly, 20 μg/5 μl, for five days) morphine (10 mg/kg, sc, 24 hrs after the last treatment with compound 48/80) showed a significant enhancement in its antinociceptive properties and a marked increase in the duration of action in both analgesic tests, compared to saline-pretreated rats. In rats pretreated with combined compound 48/80 (20 μg, icv) plus the nonsteroidal antiinflammatory drug acetylsalicyclic acid (30 mg/kg, ip. 60 min before compound 48/80) for five days, the effect of morphine (10 mg/kg, sc, 24 hrs after) was reduced both in its intensity and in its duration of analgesic efficacy, compared to saline-pretreated rats. Since in this study acetylsalicylic acid-pretreatment was shown to inhibit the morphine response in tailflick and hot-plate tests only in animals lacking in brain mast cell histamine following icv administration of compound 48/80, results suggest that cyclooxygenase products of arachidonic acid may be intermediates in the adaptive processes involved in shock/stress functional disturbances in rat brain. © 1993 Birkhäuser Verlag.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/664409
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