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)

In a randomised double-blind study of 20 patients with chronic pain, epidural morphine 5 mg in 5 ml of saline was compared with epidural clonidine 150 micrograms in 5 ml of saline. Thirteen patients had a clinical and radiological diagnosis of arachnoiditis, 6 had low back pain and 1 had post-operative scar pain. There were 18 females and 2 males with an average age of 52 years, range 22-76 years. There was no difference found between the 2 solutions in the resultant analgesia measured by the visual analogue scale for pain, pain relief or the pain word score during the 3 h period of the study. No difference was found in the patient's mood which was also measured with the visual analogue scale. Two patients had no analgesia from either injection, 2 patients did not obtain any relief from clonidine and another 2 obtained no relief from morphine. Six patients reported that clonidine was better than morphine, 5 reported that morphine and clonidine were the same and 3 reported that morphine was better than clonidine. The duration of analgesia from the clonidine varied from 6 h to 1 month; the duration of analgesia from morphine varied from 6 to 24 h. Clonidine was associated with sedation and a fall in blood pressure of greater than 20 mm Hg in all patients, 1 patient required ephedrine to treat hypotension. Twelve patients had pruritus, 7 nausea and 2 vomiting following the morphine. Statistically there was no difference found between morphine and clonidine for short-term (3 h) analgesia in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A double-blind comparison between epidural morphine and epidural clonidine in patients with chronic non-cancer pain. 317 51

In a randomized, double-blind crossover study, 40 patients with postherpetic neuralgia were given single oral doses of clonidine, 0.2 mg, codeine, 120 mg, ibuprofen, 800 mg, or inert placebo. Pain relief and side effects were recorded for 6 hours. Patients reported significantly more relief after clonidine than after the other three treatments. Codeine and ibuprofen were ineffective. Sedation, dizziness, and other side effects were more frequent after clonidine (74%) or codeine (69%) than after placebo (36%) or ibuprofen (28%). Reported pain relief was greater during trials in which side effects were present. A single, mild side effect was associated with as much additional pain relief as multiple, severe side effects. Clonidine's superiority to codeine, which had a similar incidence of side effects, argues for a specific analgesic effect. In addition, side effects may have contributed to clonidine analgesia, perhaps by suggesting to patients that they had received a potent drug.
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PMID:Association of pain relief with drug side effects in postherpetic neuralgia: a single-dose study of clonidine, codeine, ibuprofen, and placebo. 328 74

Intrathecally administered clonidine produces analgesia, but also produces hypotension. To assess the effects of epidural administration, the authors inserted lumbar epidural catheters in seven nonpregnant ewes, and injected, on separate days, clonidine (50-750 mcg), morphine (5-10 mg), and a clonidine-morphine combination (clonidine 150 mcg + morphine 5 mg). Clonidine produced dose-dependent antinociception and sedation, with the lowest maximally effective antinociceptive dose being 300 mcg. Morphine produced less intense antinociception than clonidine, and did not potentiate clonidine's effect. Antinociception, but not sedation, following clonidine injection was reversed by epidural injection of the alpha 2-adrenergic antagonist, idazoxan. Epidurally administered naloxone and prazosin did not reverse clonidine's antinociceptive effect, nor did intravenously administered idazoxan. Epidurally administered clonidine did not decrease blood pressure or heart rate or affect arterial blood gas tensions or spinal cord histology. These data suggest that epidurally administered clonidine produces analgesia by a local, alpha 2-adrenergic mechanism. In sheep, epidurally administered clonidine does not produce hypotension.
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PMID:Epidural clonidine produces antinociception, but not hypotension, in sheep. 356 15

Earlier studies have shown that the antihypertensive action of clonidine is reversed by naloxone in hypertensive (SHR), but not in normotensive rats (WKY). We investigated the effects of clonidine and naloxone on pain sensitivity of SHR and WKY by using the formalin test (FT) and the tail-flick test (TFT). Using the FT, basal pain sensitivity was similar in SHR and WKY. Clonidine produced dose-dependent analgesia (0.03-0.15 mg/kg i.p.), and it was more potent in SHR than in WKY. The effect of clonidine was partially antagonized by naloxone (2 mg/kg i.p.) in SHR, but not in WKY. Naloxone alone caused moderate analgesia in SHR and no effect in WKY. Using the TFT, SHR displayed a naloxone-reversible decrease in basal pain sensitivity, when compared to WKY. Clonidine was ineffective (WKY) or caused moderate hyperalgesia (SHR). These results indicate that the two pain tests activate different pain controlling mechanisms, with different sensitivity to the antinociceptive action of clonidine. In SHR, this action seems to involve the release of endogenous opioids.
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PMID:Naloxone reverses the antinociceptive action of clonidine in spontaneously hypertensive rats. 397 Nov 79

Clonidine, an alpha 2 adrenergic agonist, has analgesic properties and recently has been used to suppress opiate withdrawal. These two properties theoretically make it a suitable analgesic substitute in patients tolerant to opioids. The objectives of this study were to see if intrathecal clonidine is analgesic and whether it can modify morphine withdrawal at the spinal level. Rats chronically implanted with catheters in the lumbar subarachnoid space were utilized. In analgesia experiments, intrathecal clonidine produced analgesia with the peak effect in the paw-lick test occurring at 200nM, and in the tail-flick test analgesia was apparent at 100 nM and peaked at 400 nM (in 10 microL Ringer's lactate). In dependency experiments, animals dependent on morphine (300 mg X kg-1) received intrathecal clonidine 25, 50, 200 nM in 10 microliter Ringer's lactate 72 h after morphine. Following this, a naloxone challenge, 3 mg X kg-1 was administered and withdrawal assessed. Clonidine-treated animals showed significant weight loss and decrease in temperature, and those treated with high doses showed marked hypothermia and hind-limb flaccidity. Intrathecal clonidine prevented the hyperalgesia associated with opiate withdrawal but did not affect the occurrence of the majority of behavioral signs (e.g., piloerection, irritability) associated with morphine withdrawal. Intrathecal clonidine prevented the naloxone-induced increase in blood pressure during withdrawal and in animals not treated with morphine-produced hypotension. Thus, intrathecal clonidine is analgesic, and part of the antiwithdrawal action of clonidine may be exerted at the spinal level.
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PMID:Intrathecal clonidine: analgesia and effect on opiate withdrawal in the rat. 403 43

A 70 year old hypertensive patient who had undergone a gastrectomy experienced withdrawal symptoms 10 h after a second epidural injection of morphine (150 micrograms X kg-1) for postoperative analgesia. A clonidine treatment had been stopped 129 h earlier. These symptoms disappeared shortly after a third epidural injection of morphine. Clonidine was then reintroduced. The later progressive interruption of epidural morphine analgesia did not introduce any further symptoms of withdrawal. Since physical dependence on a drug is related to repeated and prolonged administration of that drug, opiate withdrawal symptoms were highly unlikely after epidural morphine used to relieve immediate postoperative pain. Abrupt discontinuation of a long-term treatment by clonidine may produce a withdrawal syndrome, but clinical and biological signs usually occur earlier than noted in this case. Recent experimental and clinical data has provided support for the existence of a complex presynaptic regulation of noradrenergic transmission in the central nervous system, both alpha 2 and opiate receptors being implicated. The activation of such presynaptic receptors inhibits further transmitter release. Suddenly stopping the chronic administration of alpha 2 or opiate agonists was responsible for a rebound excitation of these noradrenergic neurons, inducing a withdrawal syndrome. The related withdrawal symptoms may have resulted from an interaction between the discontinuation of clonidine and the decrease in morphine activity. Practitioners should be warned of this possible side-effects.
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PMID:[Withdrawal syndrome during epidural administration of morphine after stopping treatment with clonidine]. 609 36

The effects of intrathecally administered opiates (morphine sulfate and meperidine), alpha-adrenergic agonists (clonidine and ST-91) and baclofen were examined on the shock titration threshold of macaque monkeys chronically prepared with intrathecal (I) or epidural (E) catheters. Spinal opiates produced a long-lasting analgesia which was antagonized by naloxone. The order of potency was I morphine greater than I meperidine greater than E meperidine greater than E morphine. Clonidine and ST-91, also produced a dose-dependent, long-lasting elevation in the shock titration threshold, antagonized by phentolamine, but not naloxone. L-baclofen, but not D-baclofen, resulted in a dose-dependent elevation of shock titration threshold, which was not antagonized by naloxone. Repeated administration at 24-h intervals over a 7-day period of morphine, clonidine or baclofen, resulted in a significant reduction in the analgetic effects of each drug. Cross tolerance between the three classes of agents was not observed. Intrathecal co-administration of inactive doses of ST-91 and morphine resulted in a near maximal increase in the shock titration threshold, which failed to show any significant tolerance over 21 days. Intrathecal ST-91 and morphine produced no change in either muscle strength, tendon reflexes, respiratory rate, urine formation, or the ability to locomote. Baclofen, in contrast, produced a dose-dependent decrease in muscle strength. That the intrathecal drugs did not produce anesthesia was demonstrated by their failure to block the avoidance response to ensuing ear shock cued by a light tactile stimulus applied to the hind paw. These results clearly indicate that a powerful analgesia can be produced by selectively activating adrenergic, opiate, and baclofenergic receptor systems in the spinal cord.
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PMID:Studies in the primate on the analgetic effects associated with intrathecal actions of opiates, alpha-adrenergic agonists and baclofen. 611 35

The role of the neurotransmitters, norepinephrine, dopamine and serotonin in stress-induced antinociception (SIA) was examined by altering neurochemical tone with appropriate pharmacological tools. Quipazine (15.0 mg/kg, IP) a serotonin agonist, increased the peak and duration of antinociception following stress and BC-105 (3.0 mg/kg, IP), a serotonin antagonist, blocked the increase of tail-flick latency following stress. Clonidine (0.1 mg/kg, SC) an alpha 2 agonist, markedly decreased SIA whereas phenoxybenzamine (2.5 mg/kg, IP), an alpha 1 antagonist, increased the peak and duration of SIA. When dopaminergic tone was increased with apomorphine (0.05 mg/kg, SC) the increase of tail-flick latency after stress was markedly attenuated whereas blockage of dopamine receptors with haloperidol (2.5 mg/kg, IP) increased the peak and duration of SIA. Alterations of serotonergic, but not noradrenergic or dopaminergic, tone had similar effects on increased latency in tail-flick test produced by brain stimulation produced analgesia (SPA), morphine and SIA. These data support the hypothesis that alterations in tail-flick latency involves a serotonergic system.
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PMID:The role of neurotransmitters in stress-induced antinociception (SIA). 612 May 25

This study compared the responsivity of alpha 2-adrenoceptors to agonists in normotensive (WKY) and genetically hypertensive (SH) rats. Clonidine produced a greater degree of analgesia in SH as compared to WKY rats. This analgesia was antagonized by yohimbine. Neither naphazoline nor 4-hydroxy-clonidine produced analgesia in SH or WKY rats. Our results suggest that the analgesic effects of clonidine in SH rats are probably mediated by supersensitive central alpha 2-adrenoceptors.
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PMID:Supersensitivity of analgesic responses to alpha 2-adrenergic agonists in genetically hypertensive rats. 633 90

Involvement of the catecholaminergic mechanism in foot shock (FS)- and immobilized-water immersion (IW)-stress-induced analgesia (SIA) and in the development of tolerance to the effect were investigated in mice. With daily treatment with clonidine or daily exposure to stresses, tolerance developed rapidly to the analgesic effect. Clonidine-induced analgesia, which could not be antagonized by naloxone, was potentiated in the animals rendered tolerant to FS-stress, and it was attenuated in the animals tolerant to IW-SIA. On the other hand, animals tolerant to clonidine failed to show the attenuation of FS- and IW-SIA. The analgesic effect of clonidine and the development of tolerance to the effect were not influenced by reserpine. However, reserpine pretreatment completely suppressed the analgesic effect induced by FS- and IW-stresses on the 1st day; but with daily exposure to the stress, the analgesic effect gradually appeared and returned to the control level on the 5th day. These results indicate not only the differences between clonidine analgesia and SIAs but also those between each SIA. Thus, the central catecholaminergic mechanisms play an important role in these SIAs and also in the development of tolerance to the effect, although the degree of participation of these mechanisms seems to be somewhat different between FS- and IW-SIA, as indicated by the cross-tolerance between clonidine analgesia and each SIA.
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PMID:The role of the catecholaminergic mechanism in foot shock (FS) stress- and immobilized-water immersion (IW) stress-induced analgesia in mice. 654 Mar 23


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