Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous data in rats indicate that while dopamine receptor blockers like haloperidol (HAL) potentiate opiate analgesia, dopamine receptor stimulants like apomorphine reduce cold-water swim (CWS) and 2-deoxy-D-glucose (2-DG) analgesia. Yet recently, HAL and chlorpromazine (CBZ) have been shown to reduce heat and immobilization analgesia. To address these differences, the present study investigated whether HAL (10, 50, 100 microgram/kg) or CPZ (1, 3, 5 mg/kg) would potentiate or reduce the effects of morphine (MOR), CWS, 2-DG and chlordiazepoxide (CDP) upon analgesia and activity. While HAL increased jump thresholds in a dose-dependent manner, CPZ doses exerted erratic effects. MOR analgesia was potentiated by the two higher CPZ doses and by the highest HAL dose. 2-DG analgesia was potentiated by only the highest HAL dose while CDP analgesia was potentiated by the moderate CPZ dose. While all CPZ doses potentiated CWS-induced increases in jump thresholds, the lowest HAL dose reduced this effect. These effects are considered in terms of the analgesic manipulation and its magnitude of effect, the neuroleptic and its dose, the pain test, and possible concurrent effects upon activity.
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PMID:Neuroleptic and analgesic interactions upon pain and activity measures. 612 17

Seventy-six male Sprague-Dawley rats were tested in a hot-water (55 degrees +/- 0.5 degrees C) tail-flick paradigm. Tail-flick latencies (TFL) were obtained at 30 and 15 min before intraperitoneal injection of either morphine (2.5, 5.0 and 10.0 mg/kg) clonidine (25, 50, 100 and 200 microgram/kg), chlorpromazine (CPZ, 2.5 and 5.0 mg/kg), dual injections of these drug combinations, or a saline control injection. Further TFL measures were taken immediately following drug administration and thereafter at 15 min intervals. The mean of the pre-drug TFL's served as each rat's baseline. All other TFL's were calculated as percentage changes from that baseline. Mean changes were determined for each treatment group and differences between groups, at each test time, were analysed. Our results demonstrated morphine and clonidine analgesia but CPZ hyperalgesia. The drug interaction studies revealed that morphine analgesia is enhanced by co-administration of either clinidine or CPZ but that clonidine analgesia is antagonized by chlorpromazine. These data suggest that morphine and clonidine exert their analgesic effects through different neurochemical mechanisms. It is particularly interesting that the clonidine-CPZ combination should result in TFL's similar to baseline levels, even though both drugs are sedatives. The investigation emphasizes the value of chlorpromazine as a pharmacological tool in analgesic research because of its ability to induce hyperalgesia even though it is a sedating agent.
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PMID:Chlorpromazine hyperalgesia antagonizes clonidine analgesia, but enhances morphine analgesia in rats tested in a hot-water tail-flick paradigm. 681 71