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)

1. The antinociceptive effect of compound 48/80 was reversed by the pretreatment with an angiotensin-converting enzyme (ACE) inhibitor, Hoe 498, in a dose-dependent manner and with a opiate receptor antagonist, naloxone (5.0 mg/kg, s.c.) in rats. 2. The increase of plasma beta-endorphin-like immunoreactivity produced through s.c. administration of compound 48/80 was attenuated by the pretreatment with Hoe 498 but not with naloxone. 3. The present data suggest the possible involvement of renin-angiotensin system in compound 48/80-induced analgesia in rats.
Gen Pharmacol 1989
PMID:The role of renin-angiotensin system in compound 48/80-induced analgesia in rats. 252 74

1. The interactions of three GABAergic compounds, gamma-acetylenic GABA, gamma-vinyl GABA and ethylenediamine with the analgesic effects of morphine and pentazocine were examined in mice using the hot plate and tail immersion tests. 2. A significant increase in reaction time induced by morphine was noted in the tail immersion test after pretreatment with the drugs acting through GABA functions. 3. The inhibitors of GABA transaminase, gamma-acetylenic GABA and gamma-vinyl GABA, and the GABAmimetic ethylenediamine did not significantly change the analgesic action induced by pentazocine. 4. In the hot plate test the three GABAergic compounds antagonized the analgesic effects of pentazocine in contraposition with previous results indicating that morphine-induced analgesia is increased by pretreatment with those agents. 5. These findings suggest that GABAergic and opiopeptidergic systems are interconnected through mu receptors, whereas the kappa opiate systems seem to be unrelated to GABA functions.
Gen Pharmacol 1989
PMID:A comparison of GABAergic influences on the analgesic responses to morphine and pentazocine. 271 13

An acute form of "stress-analgesia" is evoked by allowing the smoke of a cigarette to envelope the nostrils of unanaesthetized rabbits. The response consists of an immediate and generalized arrest of spontaneous movements, including respiration and expiration, reduced muscular tone, and unresponsiveness to pinching. This motor "paralysis" is accompanied by a profound bradycardia. Attempts have been made to identify the neurotransmitters involved in "the smoke reflex" by the intervention of antagonists and psychopharmaca. The bradycardia was selectively blocked by atropine, leaving the somatomotor inhibition unaltered. All components of the response were abolished by approximately 60% by clonidine and by 40% by the tricyclic antidepressant amitriptyline, both of which are known to attenuate the release of noradrenaline as agonsits of alpha 2-adrenoceptors. Yohimbine blocked the clonidine effect. Naloxone (1-2 mg/kg), p-chlorphenylalanine and dexamethasone failed to influence the reflex response, suggesting that opiate, serotonergic and ACTH-systems do not play a critical role. The same applied to the benzodiazepine chlordiapoxide. The results suggest that this acute stress-induced analgesia is mediated via a noradrenergic system. The relationship of the smoke reflex to "the fear paralysis reflex", a possible trigger mechanism for the sudden infant death syndrome, is discussed.
Gen Pharmacol 1987
PMID:Neurotransmitters in "the smoke reflex" in rabbits. 288 36

1. The effect of droperidol pre-treatment on the analgesic potency of morphine, fentanyl and sufentanil was assessed in mice. 2. Acetic acid writhing test and tail immersion test were used to measure the analgesic response. 3. The neuroleptic augments the effects of sufentanil and fentanyl. 4. Thus, the dose-response curves for fentanyl and sufentanil were shifted to the left and the ED50 of the analgesics lowered in droperidol pre-treated animals. 5. However, morphine analgesia was not influenced by droperidol. 6. The results suggest that combination of sufentanil or fentanyl with droperidol may be better than morphine to produce neuroleptanalgesia and anesthesia.
Gen Pharmacol 1988
PMID:Droperidol enhances fentanyl and sufentanil, but not morphine, analgesia. 290 82

1. Intraperitoneal (i.p.) injection of different doses of baclofen (5, 7.5 and 10 mg/kg) induced analgesia in tail-flick test. The effect was dose-dependent. 2. The antinociception induced by baclofen (10 mg/kg, i.p.) was decreased in animals pretreated with bicuculline (1.5 mg/kg, i.p., 30 min), but not with naloxone (1.5 mg/kg, i.p., 30 min). 3. In picrotoxin (1 mg/kg, i.p., 15 min) pretreated mice, baclofen (5 mg/kg, i.p.) showed a significant analgesic effect. 4. Morphine (6 mg/kg, s.c.) induced analgesia which was antagonized by naloxone pretreatment (1.5 mg/kg, i.p.), while bicuculline or picrotoxin did not alter the morphine response. 5. These data suggest that a part of analgesic effect of baclofen may be mediated through GABAA receptor sites, and differs from that of morphine.
Gen Pharmacol 1988
PMID:GABAA-antagonists and baclofen analgesia. 321 82

1. Baclofen induced analgesia was confirmed by means of the mouse hot plate test. 2. Physostigmine significantly increased the response to baclofen whilst neostigmine was ineffective. Baclofen analgesia was reduced by atropine. 3. The response to baclofen was increased by the administration of tolazoline, propranolol and nadolol. In contrast, the analgesic response to morphine was attenuated by the antiadrenergic drugs phenoxybenzamine, tolazoline and nadolol.
Gen Pharmacol 1988
PMID:Influence of adrenergic and cholinergic mechanisms in baclofen induced analgesia. 334 2

The outcome of labour of 185 low-risk pregnancies at an isolated general practitioner maternity unit was compared with that for 185 comparable low-risk pregnancies at a specialist maternity hospital. No difference was found in mode of delivery or in the proportion of women requiring no analgesia, although significantly more women in the general practice group received analgesia beyond nitrous oxide. There was a significantly higher level of intervention in labour in the maternity hospital group in the form of fetal monitoring and augmentation of labour. The duration of first stage of labour was longer and meconium staining less frequent in the general practice group. Fourteen (7.6%) of the general practice group were transferred in labour to the specialist unit.The results suggest that where considerations for selection of low-risk pregnancy permit, the general practice maternity unit can provide a distinctive style of intrapartum care with minimum intervention.
J R Coll Gen Pract 1987 Nov
PMID:Comparison of outcome of low-risk labour in an isolated general practice maternity unit and a specialist maternity hospital. 350 37

The present study investigates the effects of ketamine on nociception towards chemical and thermic stimuli and on gastrointestinal transit in mice. The reversibility of these effects by the opioid antagonist naloxone (10 mg/kg) was also assessed. Ketamine promoted dose-related analgesia in both the acetic acid-induced writhing and hot plate tests. Analgesia was not influenced by pretreatment with naloxone. Contrasting the constipation induced by opioids, ketamine enhanced gastrointestinal transit in a dose-dependent manner and this was not modified by naloxone. These results suggest that although ketamine can elicit analgesia, it does not activate opioid mechanisms in subanesthetic doses.
Gen Pharmacol 1987
PMID:Effects of ketamine on nociception and gastrointestinal motility in mice are unaffected by naloxone. 356 47

Picrotoxin, an antagonist of GABA-associated chloride ionophores with convulsant activity, possesses antinociceptive activity in the hot-plate and writhing tests in the mouse. Analgesia produced by a subconvulsant dose of picrotoxin (0.75 mg/kg, s.c.) was reversed by naloxone (1.0 mg/kg, s.c.), atropine (5 mg/kg, i.p.), and methysergide (10 mg/kg, i.p.) in the jumping reaction (hot-plate test). These data indicate that opiate pathways, as well as cholinergic and serotoninergic pathways could be involved in the mechanism that underlies picrotoxin-induced analgesia. Furthermore, such results should be considered when interpreting the behavioral effects of picrotoxin.
Gen Pharmacol 1986
PMID:Antinociceptive action of picrotoxin in the mouse. 375 56

The dose-related effects of intravenously administered fentanyl (0.010, 0.005, 0.0025 mg/kg) and saline were studied in mature performance horses using a rigorous experimental protocol. Fentanyl produced a dose-related prolongation of the skin twitch reflex latency but did not increase the hoof withdrawal reflex latency. Dose related increases in stepping frequency, cardiac and respiratory rats were observed following fentanyl, while changes in rectal temperature and pupil area were not. These data indicate that fentanyl, a prototypic mu-agonist, produces a syndrome characterized by analgesia, locomotor and sympathetic stimulation in the horse.
Gen Pharmacol 1985
PMID:Dose-related effects of fentanyl on autonomic and behavioral responses in performance horses. 401 40


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