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)

Ethylenediamine, a GABA receptor agonist induced a small hyperalgesic state in mice, but increased morphine analgesia. The interaction with this morphine effect was not dose-dependent. Ethylenediamine significantly antagonized tolerance development at relatively low doses (5-10 mg/kg). The GABA mimetic agent increased the frequency of abstinence signs in the naloxone-precipitated morphine withdrawal in mice. The effect of ethylenediamine on morphine withdrawal was suppressed by the irreversible GABA transaminase inhibitor, gamma-vinyl GABA.
Gen Pharmacol 1985
PMID:Effects of ethylenediamine on morphine analgesia and tolerance-dependence in mice. 405 78

The interactions of thyrotropin releasing hormone, its metabolites and synthetic analogues with acute and chronic effects of endogenous and exogenous opiates have been described. The endogenous and exogenous opiates are represented by beta-endorphin and morphine, respectively. The pharmacological effects of opiates include analgesia, temperature effects, respiratory depression, catalepsy, locomotor activity, opiate receptor binding, tolerance, and physical dependence. Thyrotropin releasing hormone and related compounds appear to (a) antagonize hypothermia, respiratory depression, locomotor depression and catalepsy but not the analgesia induced by opiates, (b) inhibit the development of tolerance to the analgesic effect but not to the hypothermic effect of opiates, (c) inhibit the development of physical dependence on opiates as evidenced by the inhibition of development of certain withdrawal symptoms, and (d) suppress the abstinence syndrome in opiate dependent rodents. Thyrotropin releasing hormone does not interact with the opiate receptors in the brain. Potential therapeutic applications of thyrotropin releasing hormone and its synthetic analogues in counteracting some of the undesirable effects of opiates are discussed.
Gen Pharmacol 1983
PMID:Interactions of thyrotropin releasing hormone, its metabolites and analogues with endogenous and exogenous opiates. 614 Nov 21

Rats treated with phosphoramidon (an enkephalinase-inhibitor 250 micrograms, i.c.v.), morphine (20 micrograms i.c.v.) or subjected to cold-water-swim (CWS, animals forced to swim in water at 5 degrees C for 5 min) showed consistent analgesia. The antinociceptive effect of phosphoramidon, morphine and CWS was antagonised by REM sleep deprivation (REMSD). It is suggested that normal duration of REM sleep is of importance for the anti-nociceptive activity of endogenous and exogenous opiates.
Gen Pharmacol 1984
PMID:REM sleep deprivation decreases the antinociceptive property of enkephalinase-inhibition, morphine and cold-water-swim. 637 76

Episiotomy is a very common operation but little is known of its short-term or long-term morbidity.A prospective study was designed to record postpartum perineal discomfort and to investigate the presence and persistence of dyspareunia following episiotomy in 140 primigravidae. A comparison was made between those whose perineal skin was sutured with a subcuticular polyglycolic acid (;Dexon') stitch and those sutured with interrupted black silk stitches.Patients sutured with subcuticular ;Dexon' had significantly less perineal discomfort on the third, fourth, and fifth postpartum days. Patients who had epidural analgesia in labour had significantly more pain during the first five postpartum days irrespective of the suture material used.The timing of first coitus after delivery did not influence the presence or persistence of dyspareunia. Dyspareunia was commoner and lasted longer in patients sutured with ;Dexon' and it was also commoner in older primigravidae irrespective of the suture technique.
J R Coll Gen Pract 1980 May
PMID:Pain after episiotomy--a comparison of two methods of repair. 700 31

1. The effects of the substituted benzamide clebopride, an orthopramide, on nociception of chemical and thermal stimuli were investigated. 2. Clebopride (0.5, 1.0 and 2.0 mg/kg) promoted significant analgesia in the tail-flick and hot-plate tests and against abdominal constrictions produced by acetic acid or acetylcholine. 3. The analgesic effects of clebopride were not influenced by pretreatment with naltrexone (1-3 mg/kg). 4. The results suggest that clebopride induces analgesia against both thermal and chemical nociceptive stimuli, which is not mediated via opioid mechanisms.
Gen Pharmacol 1995 Sep
PMID:Antinociceptive effects of clebopride in the mouse. 755 55

1. The effect of experimental inflammation on methadone analgesia was evaluated in rats, by the tail-flick test, after single intravenous (0.35 mg/kg) and subcutaneous (3 mg/kg) doses. 2. After i.v. administration a significant decrease (P < 0.05) in the area under the methadone time-response curve was seen in rats with experimental inflammation, when compared with control. However, no differences in the analgesic response to methadone were detected between control rats and rats with inflammation when the drug was administered by s.c. injection. 3. Plasma mucoprotein levels were significantly increased (P < 0.001) and methadone free fraction was significantly decreased in rats with inflammation (P < 0.05). In addition, after i.v. methadone a decrease in brain uptake in rats with inflammation was detected. A significant correlation between brain uptake index and plasma free fraction was also observed. 4. These results suggest that a decreased immediate response to i.v. methadone may occur in circumstances in which there is an increase in alpha 1 acid glycoprotein, but that this is not likely to be observed when the absorption is not instantaneous.
Gen Pharmacol 1995 Oct
PMID:Altered methadone analgesia due to changes in plasma protein binding: role of the route of administration. 759 Jan 18

1. The analgesic effect of clonixinate of L-lysine (Clx) in the nociceptive C-fiber reflex in rat and in the writhing test in mice is reported. 2. Clx was administered by three routes, i.v., i.t. and i.c.v., inducing a dose-dependent antinociception. 3. The antinociceptive effect of Clx was 40-45% with respect to the control integration values in the nociceptive C-fiber reflex method. 4. The writhing test yielded ED50 values (mg/kg) of 12.0 +/- 1.3 (i.p.), 1.8 +/- 0.2 (i.t.) and 0.9 +/- 0.1 (i.c.v.) for Clx administration. 5. Ondansetron was not able to antagonize the antinociception response of Clx in the algesiometric tests used. 6. Chlorophenilbiguanide did not produce any significative change in the analgesic effect of Clx in the nociceptive C-fiber reflex method. 7. It is suggested that the mechanism of action of the central analgesia of Clx is not mediated by 5-HT3 subtype receptors.
Gen Pharmacol 1995 Oct
PMID:The analgesic effect of clonixine is not mediated by 5-HT3 subtype receptors. 759 Jan 33

1. The effects of acute and chronic lithium (Li+) treatments on the antinociception caused by morphine were studied in mice using the tail-flick test. 2. Subcutaneous injection of morphine (10 mg/kg) caused significant antinociception. 3. Acute Li+ administration (0.05, 0.1, 0.3, 1, 5 and 10 mg/kg, i.p.) alone had no significant antinociceptive effect but changed morphine analgesia; low doses of Li+ (0.1, 0.3 and 1 mg/kg) were found to decrease the antinociception induced by morphine whereas higher doses of the drug (10 mg/kg) potentiated this effect. 4. The 6 day administration of Li+ with a serum level of 0.528 mM decreased the antinociceptive effect of morphine. 5. The effect of Li+ on morphine-induced analgesia persisted for 96 hr in spite of the fact that Li+ drinking was discontinued (the serum Li+ level decreased from 0.528 to 0.022 mM). 6. It has been reported that Li+ might change both the binding of opioids to their receptors and biosynthesis or release of endogenous opioids. There is also a considerable body of evidence which indicates that both Li+ and morphine affect phosphoinositide turnover, intracellular calcium content and cyclic AMP level. The interaction of two drugs may conceivably take place through these systems. 7. These data suggest that the biological effects of Li+ may exist at very much lower serum Li+ levels than the commonly accepted therapeutic range.
Gen Pharmacol 1994 Dec
PMID:The effect of lithium on morphine-induced analgesia in mice. 772 Oct 39

1. When the analgesic effect of salmon-calcitonin (S-CT) and of eel-calcitonin (E-CT), as well as their influence on the morphine-analgesia were compared, no significant differences were found. 2. While on isolated tissues, E-CT induced a significant increase on the effect of bremazocine, [D-Pen2,D-Pen5]enkephalin and [Met5]enkephalin and no changes were observed on the effect of DAMGO, suggesting that E-CT increases the effects of opioids acting on delta or kappa receptors but not on mu receptors. 3. These findings corroborate the possibility of interactions between calcitonin and the opioid system.
Gen Pharmacol 1995 May
PMID:Analgesic effect of two calcitonins and in vitro interaction with opioids. 778 40

1. In male mice, 80 inescapable footshocks (S-80) induce analgesic responses measured by the tail flick test that are blocked by naloxone and the kappa opioid antagonist, nor-binaltorphimine. We now study the nociceptive responses, induced after this particular stress, measured by the writhing test, the tail immersion test and a high intensity tail immersion test both in male and female mice. 2. In stressed males, analgesic responses are seen in all the nociceptive tests. Naloxone (10 mg/kg) does not prevent them. 3. In stressed females, in contrast with males, no analgesia is produced in the tail flick test. The writhing test and the tail immersion test registered analgesic responses that were not prevented by naloxone (10 mg/kg). 4. We conclude that only the antinociceptive kappa opioid mediated component of the stress we study is strongly dependent on gender, in contrast to other types of analgesia triggered by the same stress.
Gen Pharmacol 1994 Sep
PMID:Gender and test dependence of a type of kappa mediated stress induced analgesia in mice. 783 35


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