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)

Analgesic and antipyretic activities of 2-(4-(2-imidazo-[1,2-a]pyridylphenyl)propionic acid (Y-9213) were studied with various experimental models. The analgesic activity of Y-9213 was found to be more potent than that of indometacin and morphine in the silver nitrate, Randall-Selitto, and phenylquinone writhing tests. Y-9213 also showed an analgesia in the tail pinch and electric stimulation test. On the warm water induced foot withdrawal reflex, Y-9213 was more effective in spinal-sectioned mice than in intact mice similarly to mephenesin and diazepam. Y-9213 was also proved to possess antipyretic activity as potent as indometacin and to be devoid of morphine-like property. Y-9213 exhibited little effect on the respiration and cardiovascular system in dogs. Y-9213 was found to be rapidly absorbed and eliminated from the blood with a half-life of about 2.5 h in rats. These findings indicate that Y-9213 may be an effective and well tolerated antipyretic and analgesic agent.
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PMID:The analgesic activity of imidazopyridine derivatives. 31 30

A double blind study using flurbiprofen (2-(2-fluoro-4-biphenylyl propionic acid) 150 mg daily and soluble aspirin (3.6 g daily) for 5 days immediately after injury, was carried out in 52 soft tissue injuries to the lower limb in professional sportsmen. Flurbiprofen was more effective than aspirin in producing analgesia (when daily pain scores were considered) after day 2 (p less than 0.02); and flurbiprofen produced a more effective resolution of soft tissue trauma when days to training and match play were considered (p less than 0.05). The inhibitory effects of flurbiprofen on prostaglandin biosynthesis and tissue action are mentioned and the use of anti-inflammatory agents given immediately after soft tissue injuries discussed.
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PMID:A comparative study of flurbiprofen and aspirin in soft tissue trauma. 78 22

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of oxaprozin are reviewed. Oxaprozin, a nonsteroidal anti-inflammatory drug (NSAID) under consideration for approval by the Food and Drug Administration, is characterized as a propionic acid. By inhibiting cyclo-oxygenase, oxaprozin decreases the formation of prostaglandin (PG) precursors from arachidonic acid, resulting in decreased PG biosynthesis and reduced pain and inflammatory responses. Oxaprozin is well absorbed after oral administration, and peak plasma concentration is reached in three to six hours. Oxaprozin is primarily eliminated by urinary excretion of the unchanged drug. It has a long elimination half-life and persists in synovial fluid. In clinical studies, oxaprozin was equally or more effective than aspirin and as effective as naproxen in the treatment of rheumatoid arthritis. For treatment of osteoarthritis, oxaprozin was as effective as naproxen and more effective than aspirin or piroxicam. Studies have also shown oxaprozin to be effective therapy for juvenile rheumatoid arthritis and ankylosing spondylitis. Oxaprozin, like other NSAIDs, can cause gastrointestinal adverse effects. Other possible adverse effects include allergic reactions, analgesic nephropathy, hepatotoxicity, and increased bleeding times. For adults, the anticipated daily dosage is 600-1200 mg given as a single dose for rheumatoid arthritis, osteoarthritis, and analgesia. In children, oxaprozin 10-20 mg/kg/day has been used to treat juvenile rheumatoid arthritis. Oxaprozin is as effective as other NSAIDs and offers once-daily dosing; however, it does not offer any therapeutic advantage over other currently available NSAIDs.
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PMID:Oxaprozin: a once-daily nonsteroidal anti-inflammatory drug. 845 76

Flurbiprofen (Ansaid, Upjohn), a substituted phenyl propionic acid, is a new analgesic/anti-inflammatory agent. To evaluate its relative efficacy in noninflammatory pain, 159 hospitalized women with moderate or severe postpartum uterine cramps were given single oral doses of 50 mg of flurbiprofen, 650 mg of aspirin, 60 or 120 mg of codeine sulfate, or placebo in a parallel, stratified, randomized block, placebo-controlled, double-blind trial. Patients rated pain intensity, pain relief, and side effects in uniform interviews for six hours after treatment. All measures of peak and summed analgesia exhibited significant differences among the five treatments. Flurbiprofen and aspirin showed the greatest analgesic response and were significantly superior to placebo. Results of codeine treatment were equivocal with no evidence of a positive dose response. Side effects were unremarkable except for dizziness and drowsiness after the 120-mg codeine dose. These findings suggest that flurbiprofen as an analgesic for patients with postpartum uterine pain is equivalent to aspirin and superior to codeine.
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PMID:Flurbiprofen, aspirin, codeine, and placebo for postpartum uterine pain. 351 27

Previous reports, that intrathecal morphine is more potent on the tail-flick test of acute spinal rats than intact rats, suggested that spinal opiate analgesia was attenuated by neurotransmitter release from descending pathways. To determine if this phenomenon involved excitatory amino acids (EAAs), 0.25 nm of N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) were i.t. co-administered with morphine to Intact and Spinal rats. NMDA potentiated morphine antinociception in Intact but not Spinal rats; AMPA had no effect in Intact rats, but significantly reduced morphine antinociception in Spinal rats. The data suggest a reciprocal descending, modulatory influence on the spinal interaction between EAAs and morphine.
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PMID:Intrathecal co-administration of morphine and excitatory amino acid agonists produce differential effects on the tail-flick of intact and spinal rats. 751 32

Antinociception by nonsteroidal antiinflammatory drugs, notably diclofenac and S(+)-ibuprofen, has traditionally been attributed to peripheral tissue cyclooxygenase inhibition. This study investigates the potential role of the nitric oxide system for the central antinociceptive effects of diclofenac, S(+)-, and R(-)-ibuprofen. Diclofenac and S(+)- but not R(-)-ibuprofen inhibited the behavioral response dose dependently, "biting, scratching, and licking (BSL)," induced by the spinal application of N-methyl-D-aspartate, but not that of amino-methylisoxazole-propionic acid or substance P. Diclofenac and S(+)-ibuprofen induced a parallel shift in the number of BSL responses and in the duration of the response in the behavioral model at their approximate median effective doses (diclofenac 1 mumol and S(+)-ibuprofen 5 mumol). Pretreatment with L-arginine, the natural substrate for the nitric oxide synthetase, antagonized diclofenac, and S(+)-ibuprofen-induced suppression of the biting, scratching, and licking response evoked by intrathecal N-methyl-D-aspartate. D-arginine did not antagonize the diclofenac- and S(+)-ibuprofen-induced antinociception. The study results indicate that analgesia after diclofenac and S(+)-ibuprofen involves a central mechanism which may add to the peripheral antinociceptive effect of these agents. The central action of diclofenac and S(+)-ibuprofen is partly mediated by an interaction with the N-methyl-D-aspartate receptor and nitric oxide-generating mechanisms.
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PMID:Nonsteroidal antiinflammatory drug modulation of behavioral responses to intrathecal N-methyl-D-aspartate, but not to substance P and amino-methyl-isoxazole-propionic acid in the rat. 901 80

Evidence from the last several decades indicates that the excitatory amino acid glutamate plays a significant role in nociceptive processing. Glutamate and glutamate receptors are located in areas of the brain, spinal cord and periphery that are involved in pain sensation and transmission. Glutamate acts at several types of receptors, including ionotropic (directly coupled to ion channels) and metabotropic (directly coupled to intracellular second messengers). Ionotropic receptors include those selectively activated by N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainate. Metabotropic glutamate receptors are classified into 3 groups based on sequence homology, signal transduction mechanisms and receptor pharmacology. Glutamate also interacts with the opioid system, and intrathecal or systemic coadministration of glutamate receptor antagonists with opioids may enhance analgesia while reducing the development of opioid tolerance and dependence. The actions of glutamate in the brain seem to be more complex. Activation of glutamate receptors in some brain areas seems to be pronociceptive (e.g. thalamus, trigeminal nucleus), although activation of glutamate receptors in other brain areas seems to be antinociceptive (e.g. periaqueductal grey, ventrolateral medulla). Application of glutamate, or agonists selective for one of the several types of glutamate receptor, to the spinal cord or periphery induces nociceptive behaviours. Inhibition of glutamate release, or of glutamate receptors, in the spinal cord or periphery attenuates both acute and chronic pain in animal models. Similar benefits have been seen in studies involving humans (both patients and volunteers); however, results have been inconsistent. More research is needed to clearly define the role of existing treatment options and explore the possibilities for future drug development.
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PMID:Glutamate receptors and nociception: implications for the drug treatment of pain. 1146 12

The purpose of this project was to evaluate the analgesic efficacy of misoprostol when combined with ibuprofen or diclofenac Na. Animal experiments using the inflamed rat paw formalin model suggested that misoprostol potentiates the analgesic effect of some NSAIDs (nonsteroidal anti-inflammatory drugs) including diclofenac Na but not propionic acid derivatives or opiates. The dental pain model was used to evaluate the clinical relevance of this interaction. Patients received a single oral dose of study medication following surgical removal of impacted teeth. Patients were medicated for moderate to severe postsurgical pain and then filled in an analgesic diary for a 6-h observation period. Several blood samples were taken over the observation period. In addition, microdialysis samples were taken directly from the extraction socket and were analyzed for immunoreactive prostaglandin E(2) levels. The studies were single-dose, parallel group and double-blind assays. In the first study, 70 patients received an oral dose of either placebo (n = 13), misoprostol 200 &mgr;g (n = 18), ibuprofen 200 mg (n = 19), or the combination of misoprostol + ibuprofen (n = 20). Misoprostol alone demonstrated a small analgesic effect compared to placebo. Both the ibuprofen and combination groups were substantially more effective than placebo but not different from each other. The combination group had higher ibuprofen blood levels during the first 45 min but had a lower C(max) and longer time to T(max). The second study evaluated oral doses of placebo (n = 11), misoprostol 200 &mgr;g (n = 21), diclofenac Na 50 mg (n = 18), and the combination of misoprostol + diclofenac Na (n = 20). Relative to placebo, misoprostol performance was similar to the first study. When the results of the two studies were combined, there was a small, but statistically significant, analgesic effect for misoprostol. Diclofenac Na was superior to both placebo and to misoprostol alone. The combination was the most effective treatment, and for hours 4--6 it was significantly better than diclofenac Na alone. Analysis of the blood samples showed an earlier and higher peak effect for the diclofenac Na group compared to the combination, and the combination again had a lower C(max). The microdialysis probe assays demonstrated that misoprostol depressed PGE(2) levels at the peripheral site of trauma over the first 2 h after surgery. These pilot studies used small samples, and the results only suggest trend effects. Both studies demonstrated that misoprostol 200 &mgr;g, a prostaglandin analog, does have an analgesic effect. When combined with ibuprofen, there was no potentiation of analgesia. In contrast, the combination of misoprostol + diclofenac Na demonstrated an enhanced peak effect, total effect for pain intensity difference and pain relief (sum pain intensity difference [SPID] and total pain relief [TOTPAR]), and
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PMID:The Analgesic Interaction of Misoprostol with Nonsteroidal Anti-Inflammatory Drugs. 1186 59

The interaction between electroacupuncture and an N-methyl-D-aspartic acid (NMDA) receptor antagonist, (DL-2-amino-5-phosphonopentanoic acid; AP5), or an (+/-)-alpha-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainite (AMPA/KA) receptor antagonist, (6,7-dinitroquinoxaline-2,3 (1H,4H); DNQX) administered intrathecally on carrageenan-induced thermal hyperalgesia and spinal c-Fos expression was investigated. The latency of paw withdrawal (PWL) from a thermal stimulus was used as a measure of hyperalgesia in awake rats. Intrathecal (i.t.) injection of 1 and 10 nmol AP5, but not DNQX, markedly increased the PWL of the carrageenan-injected paw. At a dose of 100 nmol, either AP5 or DNQX significantly increased the PWL of carrageenan-injected paw, with AP5 being more potent. The PWLs of the non-injected and normal saline (NS)-injected paws were not detectably affected by the administration of NMDA or AMPA/KA receptor antagonists at the doses tested. Unilateral electroacupuncture stimulation of the 'Zu-San-Li' (St 36) and 'Kun-Lun' (UB 60) acupuncture points (60 and 2 Hz alternately, 1-2-3 mA) contralateral to the carrageenan-injected paw significantly elevated the PWLs of carrageenan- and NS-injected paws. Although neither i.t. injection of 0.1 nmol AP5 nor 1 nmol DNQX alone had an effect on the PWL of the carrageenan- and NS-injected paws, both significantly potentiated electroacupuncture-induced analgesia in carrageenan-injected rats, especially 0.1 nmol AP5. Fos expression evoked by intraplantar (i.pl.) injection of carrageenan was examined in the spinal cord with immunohistochemical methods. Three hours after i.pl. injection of carrageenan, the number of Fos-like immunoreactive (Fos-LI) neurons was significantly increased in all the layers of the ipsilateral spinal cord at L(4-5), with the highest density in laminae I-II and V-VI. Intrathecally pre-administered AP5 (10 nmol) or DNQX (100 nmol) significantly reduced the total number of carrageenan-induced Fos-LI neurons. The reduction was most apparent in laminae I-II and IV-V. Similarly, following bilateral electroacupuncture stimulation of the 'Zu-San-Li' and 'Kun-Lun' acupuncture points, the numbers of carrageenan-induced Fos-LI neurons in laminae I-II and V-VI were also markedly reduced. When a combination of electroacupuncture with 10 nmol AP5 or 100 nmol DNQX was used, the level of Fos expression in the spinal cord induced by carrageenan was significantly lower than electroacupuncture or i.t. injection of AP5 or DNQX alone. These results demonstrate that electroacupuncture and NMDA or AMPA/KA receptor antagonists have a synergetic anti-nociceptive action against inflammatory pain. Furthermore, this study supports the idea that both NMDA and AMPA/KA receptors are involved in spinal nociceptive transmission in carrageenan-inflamed rats, with the former more preferentially mediating transmission of nociceptive information from cutaneous tissue.
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PMID:Excitatory amino acid receptor antagonists and electroacupuncture synergetically inhibit carrageenan-induced behavioral hyperalgesia and spinal fos expression in rats. 1240 29

Ketoprofen is a NSAIDs of the 2-aryl propionic acid class commonly used in the treatment of inflammatory rheumatic disease, acute pain and fever. Clinically, ketoprofen seems to reduce morphine requirements by 33 to 40% with ketoprofen's supposed central mechanism of analgesia. We evaluated the efficacy and safety of intravenous (IV) ketoprofen as an adjuvant to IV PCA (patient controlled analgesia) with tramadol after major gynecological cancer surgery for postoperative analgesia. Fifty patients were enrolled in this double-blinded, randomized, placebo-controlled study. Patients were allocated randomly to two groups: group I (25 patients) served as a control group, with patients receiving saline; group II (25 patients) received ketoprofen. Patients received an intravenous bolus of saline or 100 mg ketoprofen at the end of surgery. Then, PCA was given as a 20 mg tramadol bolus and 10 min lockout time. Pain relief was regularly assessed using a visual analog scale. Tramadol consumption, side-effects, and patient satisfaction were noted during the 24 hours after the surgery. No significant difference was observed in pain score, side-effects and patient satisfaction between the groups (p > 0.05). The cumulative PCA-tramadol consumption was lower in the ketoprofen-treated patients than placebo-treated patients (p < 0.05). Our results demonstrate that a single dose of 100 mg ketoprofen reduced tramadol consumption for treatment of postoperative pain after major gynecological cancer surgery.
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PMID:Adding ketoprofen to intravenous patient-controlled analgesia with tramadol after major gynecological cancer surgery: a double-blinded, randomized, placebo-controlled clinical trial. 1270 75


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