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)

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.
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PMID:Interactions of thyrotropin releasing hormone, its metabolites and analogues with endogenous and exogenous opiates. 614 Nov 21

The ability of four opiate partial agonists (buprenorphine, xorphanol, nalbuphine and butorphanol) to produce antinociception and morphine-like physical dependence was examined in the rat. For comparative purposes, morphine was also tested. Dose-response curves were constructed using the rat tail pressure test for analgesia which indicated a rank order of potency of buprenorphine much greater than morphine greater than butorphanol greater than xorphanol = nalbuphine. Assessment of primary physical dependence liability was made using the technique of chronic intraperitoneal infusion followed by precipitation of abstinence with the opiate antagonist, naloxone. The results clearly indicate that buprenorphine was not only the most potent antinociceptive agent, but also possessed the lowest incidence of physical dependence as indicated by precipitated abstinence signs. The other opiates were very much weaker as antinociceptive agents and all produced clear signs of physical dependence.
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PMID:Physical dependence induced by opiate partial agonists in the rat. 615 17

Metkephamid is an analog of methionine enkephalin that retains high affinity for the delta receptor and is a systemically active analgesic. Since it is at least 100 times more potent than morphine as an analgesic when placed directly into the lateral ventricles, and is 30 to 100 times more potent on the delta receptor and yet is roughly equipotent on the mu receptor in vitro, it is concluded that it probably produces analgesia by action on delta receptors as well as, or rather than, on mu receptors. It has less tendency to produce respiratory depression, tolerance, and physical dependence than standard analgesics, and it is presently undergoing clinical trial.
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PMID:Metkephamid, a systemically active analog of methionine enkephalin with potent opioid alpha-receptor activity. 625 56

Chlornaltrexamine (beta-CNA) a selective, long-acting irreversible opiate antagonist inhibited the analgesia, hypothermia, hypothermia tolerance and physical dependence produced by delta 9-tetrahydrocannabinol (THC) in rats. The results suggest that there are some common features between cannabis and opiates and some actions of THC may be mediated by opioid related mechanisms in the central nervous system.
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PMID:Antagonism by chlornaltrexamine of some effects of delta 9-tetrahydrocannabinol in rats. 626 44

p-Chlorophenylalanine (p-CPA) reduces brain 5-hydroxytryptamine (5-HT) without altering the dopamine and norepinephrine content. Morphine does not influence the 5-HT level, but partly reverses the depletion of 5-HT by p-CPA. Morphine analgesia and toxicity are not affected by p-CPA treatment. p-CPA also has no effect on acute morphine hypothermia, but after chronic treatment of 5-HT-deficient mice the dose--response curve is no longer parallel, which suggests that another mode of morphine hypothermia occurs. p-CPA diminishes morphine-induced running after acute as well as after chronic morphine administration. p-CPA treatment reduces the sensitivity to the naloxone-precipitated withdrawal reaction, but does not affect the development of physical dependence.
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PMID:The influence of p-chlorophenylalanine on different morphine effects. 644 58

The clinical pharmacology of the narcotic-type analgesics is discussed in depth. Relative analgesic potency, peak and duration of analgesia, oral potency, and adverse effects are reviewed, With an emphasis on the clinical application of this knowledge. The differences among psychologic dependence, physical dependence, and tolerance are carefully delineated. Guidelines are provided for using narcotic-type analgesics in the management of patients with cancer.
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PMID:Role of opioid analgesics. 648 29

The effects of taurine on the analgesic response to morphine, on the intensity of tolerance and on physical dependence were examined. Taurine induced a hyperalgesic state and attenuated morphine analgesia in mice. The hyperalgesia was maximal at a dose level of 1.5 mg/kg i.p., while the effects of higher doses (6.0 and 10.0 mg/kg) were masked by a depression of the animals' gross behavior. Taurine induced a dose related antagonism of morphine tolerance. The amino acid administered 30 min before naloxone, produced a partial reduction in the abstinence signs in the chronically treated mice. Taurine also attenuated the abstinence behavior when administered during the course of dependence. The results are consistent with taurine antagonism to the known effects of morphine on intracellular calcium disposition in nervous tissue.
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PMID:Effects of taurine on tolerance to and dependence on morphine in mice. 653 78

The experiments concerned the effects of glucuronate or sulfate conjugation at the 6-position of nalorphine on the analgesic and antagonistic activities and also on the development of tolerance and physical dependence. Nalorphine-3-and 6-sulfate ester were synthesized for the first time. The analgesic effect of nalorphine-6-sulfate and -glucuronide was higher than that of nalorphine when assessed in the acetic acid writhing test. However, these 6-conjugates exhibited less potent agonistic activity in the test with guinea-pig ileum muscle strip and revealed no analgesic effect in the tail pinch test. The antagonistic activity of these 6-conjugates to morphine analgesia was lower on their s.c. injection, but higher on i.c.v. injection than that of nalorphine. The development of tolerance to the analgesia caused by nalorphine was not affected by the 6-modifications. Frequent withdrawal signs were seen in mice treated chronically with anlorphine-6-conjugates by challenging with naloxone while mice treated with nalorphine showed no such signs. This potent enhancing effect of 6-conjugation on the development of physical dependence was suggested to be also the case with morphine. These changes of potency due to conjugation were interpreted as due to the altered interaction with multiple opioid receptors.
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PMID:Potentiation of physical dependence by conjugation at the 6-position of nalorphine. 654 Nov 41

Electrical stimulation of the brainstem abolishes pain, while continued stimulation induces tolerance to the analgesic effect. Analgesic drugs producing tolerance also induce physical dependence, suggesting that the phenomenon of tolerance is associated with addiction. There is evidence that the neural mechanism for stimulation-produced analgesia is related to the release of opiate substances within the brain. We therefore propose that repeated or protracted brain stimulation elicits dependence upon the endorphins released by electrical stimulation of the neurons themselves. To investigate this possibility, rats were given repetitive bursts of analgesic electrical brain stimulation for two hours. Immediately thereafter, they were injected with the opiate antagonist, naloxone. Behaviors associated with low grade opiate withdrawal were observed. These data suggest that prolonged analgesic stimulation can result in naloxone-precipitated behaviors similar to the behaviors exhibited during opiate withdrawal.
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PMID:Opiate withdrawal behavior after focal brain stimulation. 654 76

Chronic morphine treatment (subcutaneous pellet implantation of four morphine pellets) caused significant tolerance to morphine analgesia as observed at zero and 6 hrs. after pellet removal. However, such treatment failed to elicit any changes in striatal muscarinic receptors using (3H)-QNB binding studies. At 24 hours after pellet removal there was significant development of physical dependence but the affinity (Kd) as well as density (Bmax) of striatal muscarinic receptors remained unaffected. Although naloxone caused marked precipitation of abrupt withdrawal in morphine tolerant rats, it also failed to produce any changes in striatal muscarinic receptors. Results indicate that any cholinergic involvement in opiate tolerance and physical dependence does not involve an effect on muscarinic receptors.
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PMID:The binding of 3H-quinuclidinyl benzilate to cholinergic muscarinic receptors in rat brain region following chronic treatment with morphine and during abstinence. 654 85


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