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)

Analgesia (NAA) caused by nonacupuncture point (abdominal muscle) stimulation after lesioning the analgesia inhibitory system (AIS) or treating the subject with proglumide was abolished by hypophysectomy or adrenalectomy. The final sector of the NAA afferent pathway from the nonacupuncture point to the pituitary gland and the initial sector of the descending pain inhibitory system were found in the anterior and posterior arcuate nucleus (A-HARN and P-HARN), respectively. Analgesia caused by ACTH microinjected into the P-HARN disappeared after denervation of the A-HARN, but that caused by dopamine did not. Firing rates of P-HARN neurons were increased by nonacupuncture point simulation (NAPS) after lesion of the AIS or treatment with proglumide. The NAPS responsive neurons also responded to ultramicroinjected dopamine, but not to ultramicroinjected ACTH. Both NAA and NAPS responsive neuron activity that were abolished by hypophysectomy were restored by concurrent application of NAPS and intraperitoneal ACTH. Reduction of sodium ions due to adrenalectomy was found to abolish NAA. It was concluded that NAA production involves dopaminergic transmission in the HARN and ACTH acting presynaptically on this transmission.
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PMID:Analgesia produced by pituitary ACTH and dopaminergic transmission in the arcuate. 165 17

A comparison of plain prilocaine and bicarbonated prilocaine in intravenous regional anesthesia was studied in 30 patients undergoing upper extremity surgery. The patients were divided into two groups: one group was given anesthesia in the form of 1% prilocaine and the other group was given 1% prilocaine plus sodium bicarbonate. The onset of analgesia and anesthesia and recovery from analgesia and anesthesia were investigated in both groups. Bicarbonated prilocaine produced faster onset of analgesia when compared with plain prilocaine (P less than 0.01). The onset of anesthesia and recovery from analgesia and anesthesia were not statistically different between the two groups. Clinically, the intensity of anesthesia was better when bicarbonated prilocaine solution was used instead of plain prilocaine. We conclude that bicarbonated prilocaine is better than plain prilocaine during IVRA.
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PMID:The addition of sodium bicarbonate to prilocaine solution during i.v. regional anesthesia. 166 29

We have previously described the peripheral analgesic effect of dibutyryl cyclic GMP, acetylcholine (ACh) and morphine (Mph) injected into the rat paws. Since ACh induces nitric oxide (NO) release from endothelial cells which is though to stimulate guanylate cyclase (GC) we investigated if NO-cyclic GMP pathway was involved in the analgesia by those agents. Using a modification of the Randall-Selitto rat paw test, it was found that sodium nitroprusside, which releases NO non-enzymatically, blocked rat paw PGE2 induced hyperalgesia. The peripheral analgesic effect of sodium nitroprusside, ACh and morphine was enhanced by intraplantar injection of an inhibitor of cyclic GMP phosphodiesterase (MY5445) and blocked by a GC inhibitor, methylene blue (MB). Peripheral analgesia induced by ACh and morphine, but not by sodium nitroprusside, was blocked by NG-monomethyl-L-arginine (L-NMMA) an inhibitor of the formation of NO from L-arginine. Central effect of morphine as tested by the rat paw and by the tail flick tests was inhibited by intraventricular injection of methylene blue. In addition, the central morphine analgesia was potentiated by My5445. In contrast, with the periphery, the central effect of morphine was not blocked by L-NMMA. Our results demonstrate that NO causes peripheral analgesia via stimulation of GC and supports the suggestion that at this site morphine and acetylcholine analgesia is subsequent to NO release. In the mechanism of the central analgesic effect of morphine, the cGMP system is activated but via NO release, probably by a direct stimulation of the receptors. This is the first demonstration that links peripheral and central analgesic effect of morphine to the stimulation of GC system.
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PMID:Molecular base of acetylcholine and morphine analgesia. 167 74

Experimental studies have shown that opioids could produce two types of effect on neuronal excitability. The first one, aspecific, is a local anesthetic action on the nerve fiber with a diminution of sodium and potassium conductance. The second is specific: the sodium conductance lowering is due to a linkage of the opioid with a receptor on the internal face of the membrane. Opioids could also migrate to the posterior horn of the spinal cord after linkage with axonal receptors. Clinical studies have proved that opioid injection in peripheral nervous trunks and specially in the brachial plexus produce a prolonged analgesia status in the post operative period but also and mostly in the chronic pain. The more liposoluble opioids like fentanyl and buprenorphine are the more effective.
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PMID:[Mechanism of action and clinical use of opioids administered by the peripheral perineural route]. 167 79

Forty patients were studied at precisely timed 10 min intervals during transurethral prostatic resection under epidural analgesia. Blood gases, serum sodium, and volumetric irrigating-fluid balance were measured. A decrease in the serum sodium level of less than 5 mmol litre-1 was recorded in 28 patients (the 'normal TUR' group). In 12 patients, the decrease was 5 mmol litre-1 or more, which corresponded to an average absorption of irrigant of 1 litre of 2.2% glycine solution (range 0.6-2.9; the 'absorption' group). Mild metabolic acidosis often developed during the operations, but this was of similar degree in the two groups. It was concluded that uptake of irrigating fluid containing glycine does not alter the acid-base status so long as the TUR syndrome does not develop.
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PMID:Acid-base status following glycine absorption in transurethral surgery. 173 93

Intramuscular (i.m.) and intravenous (i.v.) administration of detomidine at doses of 10, 20 and 40 micrograms/kg body mass was evaluated for its sedative and analgesic properties in 15 goats (Capra hircus). The drug produced dose- and route-dependent sedation. The 10 micrograms/kg dose was effective only when administered i.v. There was no observable analgesia at this dose. Higher doses produced effective sedation and moderate analgesia of the body with either route of administration. Severe ataxia and sternal recumbency were seen in all the animals after the dose of 40 micrograms/kg. Other effects of detomidine in these goats included mild to moderate salivation, depressed respiratory rate, decreased rectal temperature, bradycardia and hyperglycaemia. Plasma concentrations of total protein, sodium, potassium and chloride were not affected.
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PMID:Evaluation of detomidine as a sedative in goats. 178 30

Meclofenamic acid is a nonsteroidal anti-inflammatory drug (NSAID) approved for use in arthritis (osteo and rheumatoid), analgesia (mild to moderate pain), dysmenorrhea, and heavy menstrual blood loss (menorrhagia). At least three different biochemical effects have been defined for meclofenamic acid. It is a potent inhibitor of the enzyme cyclooxygenase, thereby inhibiting the production of prostaglandins. It also inhibits the release of 5-HETE and LTB4 from human neutrophils stimulated with calcium ionophore and antagonizes the response of tissues to certain prostaglandins. These mechanisms may explain in part the pharmacological profile and clinical effectiveness of this compound. The rapid onset of activity of meclofenamic acid and its duration of action may be the result of its pharmacokinetic profile. Sodium meclofenamate is completely bioavailable from capsules relative to an oral suspension dosage form. Maximum meclofenamic acid plasma concentrations are achieved in 0.5-2 h following doses of capsules. Meclofenamic acid is extensively metabolized. One of the metabolites, metabolite 1, is approximately 20% as active as the parent compound in inhibiting cyclooxygenase activity in vitro. This metabolite accumulates in plasma during repeated dosing. It is possible that this metabolite may contribute to at least some of the activity observed following administration of sodium meclofenamate.
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PMID:Pharmacology, pharmacokinetics, and therapeutic use of meclofenamate sodium. 181 May 20

Good dental analgesia requires drugs that are endowed with strong and fast activity and that are well tolerated. In addition, optimal analgesia should essentially be of the peripheral type, thereby eliminating the risk of sedation that may cause unpleasant effects on the patient's daily life. Meclofenamic acid is among those substances whose analgesic effect is more evident than that of anti-inflammatory action. The mechanism of action of meclofenamic acid makes it distinctly different from other nonsteroidal anti-inflammatory drugs (NSAIDs) in that it inhibits the metabolic pathways of arachidonic acid and, at the same time, antagonizes the effects of prostaglandins at the peripheral receptor level. A number of controlled clinical trials showed that meclofenamic acid is an excellent analgesic, offering good tolerability when used in oral surgery, dysodontiasis, avulsion of the third impacted molar, and periodontitis. The following report is a presentation of results obtained in a controlled clinical trial in which the speed of pain relief was assessed in 20 patients suffering from acute periodontitis. The patients were treated orally with a single dose of meclofenamate sodium (100 mg) or with piroxicam-beta-cyclodextrin (20 mg). The intensity of the drug's analgesic effect was measured at 0.5, 1, 2, 4, and 6 h after administration. After initial testing, meclofenamate sodium was found to be significantly more effective than piroxicam-beta-cyclodextrin. Both the physician and patient found this drug to be considerably better. Pain relief after treatment with meclofenamate sodium was clinically and statistically faster than piroxicam-beta-cyclodextrin, and both drugs were found to be well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience in the treatment of dental pain. 181 May 25

Acupuncture analgesia (AA) caused by low frequency stimulation of the acupuncture point (AP) was abolished by hypophysectomy and adrenalectomy. Termination of the AA producing pathway from the AP to the pituitary gland was in the medial hypothalamic arcuate nucleus (M-HARN). The origin of the descending pain inhibitory system associated with AA was in the posterior HARN (P-HARN). AA in the hypophysectomized rats, and enhanced neuronal activity in the P-HARN that were abolished during acupuncture stimulation, were both restored by intraperitoneal microinjection of 0.5 mg/kg morphine or 0.1 micrograms beta-endorphin into the P-HARN during acupuncture stimulation. Of the analgesia produced by dopamine or beta-endorphin injected into the P-HARN, that caused by beta-endorphin disappeared after denervation of the M-HARN. The P-HARN neurons that responded to acupuncture stimulation also responded to iontophoretic dopamine, but not to iontophoretic morphine nor ultramicroinjected beta-endorphin. The transmission between the M-HARN and P-HARN may be dopaminergic, and beta-endorphin might presynaptically modulate this transmission. Reduction of sodium ions may have been the reason for abolition of AA after adrenalectomy.
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PMID:Dopaminergic transmission in the hypothalamic arcuate nucleus to produce acupuncture analgesia in correlation with the pituitary gland. 184 81

We have previously described the analgesic effect of dibutyryl cyclic GMP or acetylcholine (ACh) injected into rat paws. Since ACh induces nitric oxide (NO) release from endothelial cells, we investigated the possible involvement of the NO-cyclic GMP pathway in ACh-induced analgesia, using a modification of the Randall-Selitto rat paw test. We found that sodium nitroprusside, which releases NO non-enzymatically, caused antinociception in the rat paw made hyperalgesic with prostaglandin E2. The analgesic effect of sodium nitroprusside and ACh was enhanced by intraplantar injection of an inhibitor of cyclic GMP phosphodiesterase (MY 5445) and was blocked by a guanylate cyclase inhibitor, methylene blue (MB). The analgesia induced by ACh, but not by sodium nitroprusside, was blocked by NG-monomethyl-L-arginine (L-NMMA), an inhibitor of the formation of NO from L-arginine. L-arginine itself had little or no effect upon prostaglandin-induced hyperalgesia but caused significant analgesia in paws inflamed with carrageenin. This analgesia was blocked by MB, as well as by L-NMMA, and was potentiated by MY 5445. These results suggest that ACh-induced analgesia was mediated via the release of NO. The results also indicate that the guanylate cyclase system is stimulated in the inflammatory reaction. The analgesia resulting from activation of this system is possibly overshadowed by substances that concomitantly stimulate nociceptor hyperalgesic mechanisms.
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PMID:Peripheral analgesia and activation of the nitric oxide-cyclic GMP pathway. 198 Nov 87


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