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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Caffeine has been found to potentiate the acute anti-inflammatory activity of aspirin, indomethacin, and phenylbutazone, but not the activity of sodium salicylate or hydrocortisone, in the carrageenan pleurisy or hindlimb models of inflammation in the rat. The mobilization of inflammatory cells was not affected by aspirin in the presence or absence of caffeine. The mild analgesia produced by aspirin was confined to a hyperalgesic test in which this drug was able to reduce inflammation and concomitant hyperalgesia and thereby produce an "apparent" analgesic effect. This "apparent" analgesia produced by aspirin was potentiated by caffeine. The mechanism responsible for the potentiated anti-inflammatory and mild analgesic activity of aspirin remains unknown since caffeine did not alter the plasma salicylate levels or prostaglandin synthetase inhibition produced by aspirin.
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PMID:Potentiation of the anti-inflammatory and analgesic activity of aspirin by caffeine in the rat. 81 13

Intrathecal administration of substance P at the lower thoracic spinal level has an antinociceptive effect on reaction time in the tail-flick test; this response is blocked by naloxone i.v. but not by i.v. administration of opiate antagonists which do not cross the blood-brain barrier. As morphine-induced analgesia is blocked by adenosine antagonists, to determine whether this substance P-induced, opioid-mediated antinociception also includes a purine link, the adenosine receptor antagonist, caffeine, was given systemically 10 min prior to substance P administration. In control rats pretreated with saline, substance P (6.5 nmol) produced an increase in reaction time to about 160% of preadministration values at one min after intrathecal injection. The effect could also be observed at 6 min after this injection. Pretreatment with 16 or with 32 mg/kg of caffeine i.p. blocked the response to substance P, and produced a hyperalgesia similar to that reported in studies at the lumbo-sacral spinal level. These results indicate that the adrenal opioid-induced antinociception observed upon intrathecal administration of substance P at the lower thoracic level occurs via an adenosine link. This is the first demonstration of a purine link in the expression of antinociceptive effects of an endogenously released opioid.
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PMID:Adenosine receptor link in an adrenal opioid-induced antinociception in the rat tail-flick test. 137 72

In a randomised, double-blind, double-dummy, multiple dose, crossover study in 30 patients we compared an ibuprofen/codeine combination (400 mg ibuprofen/25.6 mg codeine phosphate) with a paracetamol/codeine/caffeine combination (1 g paracetamol/16 mg codeine phosphate/60 mg caffeine) for pain relief over 6 days after two-stage bilateral lower third molar removal. The ibuprofen combination produced significantly greater analgesia than the paracetamol combination, both on single-dose analysis of the first and second days and on multiple-dose measures for days 1, 2, 3 and 4. The mean incidence of adverse effects over the 6 days was 20% for both combinations. This trial design (crossover with multiple dosing in outpatients) is a sensitive way of testing for analgesia, and is potentially more predictive of adverse effect problems than single-dose studies. It confirms that multiple dosing may show increased efficacy.
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PMID:A multiple dose comparison of combinations of ibuprofen and codeine and paracetamol, codeine and caffeine after third molar surgery. 151 16

Recent studies have demonstrated that caffeine acts as an analgesic adjuvant when combined with acetaminophen, aspirin, or their mixture. Our objective was to determine whether similar enhancement of analgesia could be demonstrated when caffeine is combined with ibuprofen. On a double-blind basis, a single oral dose of ibuprofen (50, 100, or 200 mg), a combination of ibuprofen, 100 mg, with caffeine, 100 mg, a combination of ibuprofen, 200 mg, with caffeine, 100 mg, or placebo was randomly assigned to 298 outpatients with postoperative pain after the surgical removal of impacted third molars. With a self-rating record, subjects rated their pain and its relief hourly for 8 hours. All active treatments were significantly superior to placebo, and the caffeine effect was significant for every measure of analgesia. Relative potency estimates indicated that the combination was 2.4 to 2.8 times as potent as ibuprofen alone. The combination also had a more rapid onset and longer duration of analgesic action. The analgesic adjuvancy of caffeine clearly extends to combinations with nonsteroidal anti-inflammatory drugs other than acetaminophen or aspirin.
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PMID:Effect of caffeine on ibuprofen analgesia in postoperative oral surgery pain. 206 Feb 56

Four common oral analgesics were tested in a single-blind trial to determine their relative efficacy in the management of postsurgical pain in 103 patients who had their impacted third molars surgically removed under general anesthesia. The analgesics tested were acetylsalicylic acid (26 patients), ibuprofen (26 patients), a paracetamol/codeine/caffeine combination (Solpadeine) (25 patients), and dihydrocodeine (26 patients). The paracetamol/codeine/caffeine combination, ibuprofen, and acetylsalicylic acid preparations produced equally effective analgesia. Dihydrocodeine was found to be a poor analgesic in this pain model. There were no adverse reactions to any of the preparations.
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PMID:A study of the comparative efficacy of four common analgesics in the control of postsurgical dental pain. 223 74

1. The analogs of adenosine D- and L-phenylisopropyladenosine (D- and L-PIA) and chloroadenosine (CADO) induced analgesia in mice (hot-plate test). 2. The antinociceptive effects of the three adenosine agonists were antagonized by caffeine but were unaffected by naloxone. 3. Morphine-induced antinociception was increased by pretreatment with adenosine agonists. 4. Whereas CADO significantly attenuated the induction of morphine tolerance, D- and L-PIA did not affect the process.
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PMID:Effects of some adenosine analogs on morphine-induced analgesia and tolerance. 227 94

The effect of adenosine, S-phenylisopropyladenosine (S-PIA) and dipyridamole (an adenosine reuptake inhibitor) on the analgesic action of morphine in mice and rats was investigated in the hot-plate (56 degrees C) and tail immersion (52 degrees C) tests. Adenosine, 50 and 100 mg/kg, induced analgesia in mice and rats in the hot-plate test and potentiated the action of morphine (particularly in mice). The analgesic effects of adenosine were completely abolished by caffeine (10 mg/kg in mice and rats), and partially inhibited by naloxone (1 mg/kg, only in mice). S-PIA given alone (0.6 mg/kg) produced in mice some analgesic effect in the hot-plate test: the effect was abolished by caffeine and partially by naloxone. The effect of S-PIA on the action of morphine depends on the dose and the animal species. Dipyridamole alone did not affect the reactivity of animals in tests for analgesia, but potentiated the action of morphine.
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PMID:The effect of adenosine receptor agonists on analgesic effects of morphine. 228 Oct 16

Adenosine-mediated analgesia and interactions between opioids and adenosine in the brain have been observed by several researchers. Our investigations were designed to examine opioid-adenosine interactions at spinal sites and possible modulation of opioid-stimulated descending antinociceptive pathways by adenosine in the spinal cord. Methylxanthines administered intrathecally (i.t.) were used as adenosine receptor antagonists to determine possible interactions between opioids and endogenous adenosine. Theophylline administered i.t. dose-dependently antagonized analgesia induced by morphine administered i.t. or i.c.v. as measured by tail-flick and hot-plate assays. Analgesia induced by i.t. injections of 2-chloroadenosine, an adenosine agonist, was also antagonized by theophylline. However, doses of naloxone (i.t.) that antagonized analgesia induced by i.t. injections of morphine had no effect on 2-chloroadenosine (i.t.)-induced analgesia. These data support morphine-stimulated release of adenosine in the spinal cord. Antagonism of morphine (i.c.v.)-induced analgesia by theophylline was mimicked by caffeine and isobutylmethylxanthine. The results could not be explained as a consequence of effects on phosphodiesterease enzymes, drug-induced hyperalgesia or spinal redistribution of i.c.v. administered morphine. Therefore, our studies suggest that endogenous adenosine in the spinal cord is involved in analgesia mediated by opioid-stimulated descending antinociceptive pathways.
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PMID:Spinal adenosine modulates descending antinociceptive pathways stimulated by morphine. 242 75

The role of spinal manipulation in the relief of pain is becoming clearer and more demonstrable as time passes. One approach to this study is the effect of manipulation on the neurochemical mechanisms of antinociception. Chief among these is beta-endorphin, which has been found to produce a wide range of beneficial effects, especially analgesia. The intent of our study was to demonstrate the effect of spinal manipulation on plasma beta-endorphin levels. Three groups of male subjects were randomly created: the experimental, sham and control groups. All three groups were screened for symptomatology, present use of medications and the present use of innocuous stimulants, such as nicotine and caffeine. A standard protocol involving a 20-min pretest resting period, an intervention and a 40-min test period ensued. The experimental group received a manipulation in the region of the cervical spine; the placebo group received a sham maneuver with no dynamic thrust; the control group received no intervention. Samples were taken by venipuncture at -20, -5, +5, +10 and +30 min. The data were analyzed by repeated measures analysis of variance and by Scheffe's post-hoc multiple comparison tests. Plasma beta-endorphin levels were assessed by radioimmune assay technique (according to the method described by Harber and Sutton in 1984). The results of our study demonstrated a small, but statistically significant, increase in serum beta-endorphin levels in the experimental group at the 5-min postintervention point. The levels in the placebo and control groups demonstrated a steady decrease that was distinct from the response in the experimental group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spinal manipulation and beta-endorphin: a controlled study of the effect of a spinal manipulation on plasma beta-endorphin levels in normal males. 294 18

(-)-N6-(R-phenylisopropyl)-adenosine (PIA) was shown to possess analgesic activity in both the tail flick and acetic acid writhing assays. The analgesic actions of PIA were antagonized by caffeine in a dose-dependent manner. An apparent pA2 analysis in vivo suggested that the antagonism by caffeine was not competitive. Subanalgesic doses of PIA potentiated morphine-induced analgesia, tolerance and dependence. Caffeine antagonized these effects of morphine. PIA attenuated while caffeine exacerbated opiate withdrawal. While a low dose of caffeine antagonized PIA effects on withdrawal, a low dose of PIA did not antagonize the effects of caffeine. These results indicate that PIA can facilitate, and caffeine can antagonize the actions of morphine and that caffeine may be exerting some of its actions independent of adenosine receptor antagonism.
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PMID:Effects of (-)-N6-(R-phenylisopropyl)-adenosine (PIA) and caffeine on nociception and morphine-induced analgesia, tolerance and dependence in mice. 299 93


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