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)

1. Receptive fields (RFs) of neurons in the primary somatosensory (SI) cortex were defined before, during, and after electrical stimulation of myelinated fibers in the dorsal cutaneous branch of the ulnar nerve in adult pentobarbital sodium-anesthetized cats. 2. This stimulation resulted in an approximately threefold increase of SI multiunit RF sizes. Substantial changes were first recorded within 1-2 h of stimulation. RFs typically enlarged continuously over a several-hour stimulation period, then stabilized. 3. RF-area increases were observed within both the forepaw and hindpaw representational zones in the SI cortex contralateral to the stimulated forepaw nerve. RF sizes did not increase in the ipsilateral SI body surface representation or in sham-stimulation control animals. 4. Preliminary studies indicate that stimulation-induced changes can be halted and often reversed by the intravenous administration of the opiate antagonist naloxone. 5. These observations suggest a global naloxone-sensitive modulatory system that operates on large-diameter afferent inputs in the cat somatosensory system. The increases in RF size occur under nerve-stimulation conditions similar to those that result in the generation of widespread analgesia (Chung et al. 1984a,b; Gamble and Milne 1986; Toda and Ichioka 1978).
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PMID:Receptive-field changes induced by peripheral nerve stimulation in SI of adult cats. 235 70

Using a within-subject, crossover experimental design, this study compared the efficacies of a nonsteroidal anti-inflammatory drug, naproxen sodium, 550 mg, administered either 30 minutes preoperatively or 30 minutes postoperatively to 36 patients undergoing the removal of impacted third molar teeth. Pain intensity was assessed postoperatively for 8 hours. Treatment with naproxen sodium, 550 mg, 30 minutes following completion of surgery was just as effective as presurgical administration in controlling postoperative pain. Administration of naproxen sodium in the immediate postoperative period may be indicated for optimum postoperative analgesia for patients in whom preoperative oral intake is contraindicated.
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PMID:A comparison of preoperative and postoperative naproxen sodium for suppression of postoperative pain. 235 42

When isobaric spinal anesthesia is applied the level of analgesia is of special interest. This level is influenced by many factors of varying importance. One major factor is the relation between cerebrospinal fluid (CSF) density and the density of local anesthetic solutions. The density of CSF changes with the concentrations of its constituents, e.g., glucose or protein. Because glucose concentrations in CSF change in parallel with blood glucose levels, this may have effects on CSF density and the spread of spinal anesthesia. In 43 patients in two groups (diabetic n = 32, non-diabetic n = 11) the influence of CSF density on the analgesia level achieved with isobaric spinal anesthesia was investigated with special reference to increased glucose levels in blood and CSF. The influence of body height and weight, age and CSF protein content were also studied. There were no statistically significant correlations between any of these factors and the extension of analgesia. The mean blockade level was 1.6 segments lower in the non-diabetic group: this difference was statistically not significant (P greater than 0.05). Anesthesia spread faster in the diabetic group, but this difference was also not significant (P greater than 0.05). For bupivacaine 0.5% alone a density of 1.0010 g/cc was found, while for bupivacaine 0.5% with epinephrine (1:200,000) the density measured was 1.0022 g/cc. There is no correlation (r2 = 0.083) between CSF glucose concentration and CSF density, other factors such as sodium, chloride or CO2, apparently being more important. With CSF density ranging between 1.000 and 1.003 g/cc there was no correlation with the blockade level (r2 = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Do elevated blood and cerebrospinal fluid glucose levels and other factors modify the density of cerebrospinal fluid and the spread of isobaric spinal anesthesia?]. 237 35

Increasing the pH of local anesthetics with sodium bicarbonate has been reported to hasten their onset of action. The purpose of this study was to compare the onset and duration of epidural analgesia with the use of sodium bicarbonate and tromethamine to increase the pH of 2% chloroprocaine (2CP). Five groups of patients were studied: Group I received 2CP; Group II received 2CP buffered to a pH of 7.1 with tromethamine; Group III received 2CP buffered to a pH of 7.1 with sodium bicarbonate; Group IV received 2CP buffered to a pH of 7.7 with tromethamine; and Group V received 2CP buffered to a pH of 7.7 with sodium bicarbonate. The final pH and PCO2 of each solution were measured. Time to onset of analgesia was significantly delayed with either of the tromethamine buffered groups (II [5.6 +/- 1.0 minutes] and IV [5.4 +/- 0.4 minutes]) when compared with data from the unbuffered control (I [4.4 +/- 0.1 minutes]) and the sodium bicarbonate buffered (III [4.5 +/- 0.8 minutes] groups and Group V [2.7 +/- 0.9 minutes]). Only when sodium bicarbonate buffer adjusted to pH 7.7 (Group IV) was onset significantly more rapid than the unbuffered 2CP (I) and tromethamine buffered 2CP (II and IV). Multiple regression analysis revealed that onset times were significantly related to both pH and PCO2. The coefficient of determination for this model was 0.5156.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of pH and PCO2 on epidural analgesia with 2% 2-chloroprocaine. 249 58

The effect of GABA agonists, namely gamma aminobutyric acid, muscimol, sodium valproate and baclofen was studied on radiant heat-induced nociception in mice. All of the drugs, with the exception of sodium valproate, enhanced the reaction time to radiant heat as effect per se. Concomitant administration of any of these agents with morphine showed a potentiation of morphine-induced analgesia. The GABA antagonists bicuculline and picrotoxin failed to reverse the antinociceptive effect; paradoxically both these agents showed antinociceptive effect per se and also enhanced the response due to morphine.
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PMID:GABAergic agents-induced antinociceptive effect in mice. 251 84

The periaqueductal gray (PAG) region of the midbrain has been implicated in both stimulation-produced and opioid-induced analgesia. High affinity mu-selective opioid binding sites presumably associated with mu-type opioid receptors have been detected in rat PAG-enriched P2 membrane. In the present study the signal transduction mechanism of mu-type opioid receptors in the PAG was examined utilizing both in vitro radioligand binding and GTPase assays. The non-hydrolyzable guanine triphosphate (GTP) analog guanyl-5'-yl beta-gamma-imidodiphosphate (GppNHp) inhibited specific high affinity [3H][D-Ala2,N-MethylPhe4,Glyol5]enkephalin (DAGO) binding in rat PAG-enriched P2 membrane in a dose-dependent manner. DAGO stimulated total GTPase activity in rat PAG-enriched P2 membrane in a saturable, dose-dependent, ligand-selective, stereoselective, and naloxone-reversible manner. This DAGO stimulation of total GTPase activity was also dependent on Na+ and Mg2+, and was abolished by pertussis toxin pretreatment of the membrane. Overall these data suggest that mu-type opioid receptors in the PAG are coupled to guanine nucleotide binding proteins (G proteins).
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PMID:Mu-type opioid receptors in rat periaqueductal gray-enriched P2 membrane are coupled to guanine nucleotide binding proteins. 253 74

A randomized, double-blind study was performed to determine whether pH-adjustment of 2-chloroprocaine hastens the onset of epidural analgesia, and improves the quality and duration of subsequent epidural bupivacaine analgesia during labor. One milliliter of either 8.4% sodium bicarbonate or normal saline was added to a 30-ml vial of 2% 2-chloroprocaine. At 0, 5, and 7 min, each patient received 2, 5, and 3 ml of 2-chloroprocaine, respectively. At 22 min, any patient who did not yet have satisfactory analgesia received an additional 5 ml of 2-chloroprocaine. At 35, and, again, at 36 min, each patient received 5 ml of 0.25% bupivacaine. The median onset of 2-chloroprocaine analgesia was slightly more rapid in the bicarbonate group than in the saline-control group (12 versus 14 min, P less than .05). Two of 31 women in the bicarbonate group, versus 10 of 31 women in the saline-control group, required an additional 5 ml of 2-chloroprocaine at 22 min to achieve satisfactory analgesia (P = .01). There was no significant difference between groups in median duration of subsequent bupivacaine analgesia (60 min in each group) or mean (+/- SD) dosage of bupivacaine during the first stage of labor (64 +/- 43 versus 72 +/- 57 mg). Also, there was no significant difference between groups in pain scores over time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of pH-adjusted 2-chloroprocaine on the quality and duration of subsequent epidural bupivacaine analgesia during labor: a randomized, double-blind study. 253 94

The periaqueductal gray (PAG) region of the midbrain has been implicated in both stimulation-produced and opioid-induced analgesia. High-affinity mu-selective opioid-binding sites associated with mu type opioid receptors have been detected in rat PAG-enriched P2 membranes, and these receptors have been shown to be coupled to guanine nucleotide-binding proteins (G-proteins). In the present study the potential G-protein-mediated coupling of mu type opioid receptors to the inhibition of adenylyl cyclase was examined utilizing in vitro adenylyl cyclase assays. In the presence of Na+, opioid agonists inhibited adenylyl cyclase in a mu selective, naloxone reversible, dose dependent, and pertussis toxin sensitive manner. Overall the data suggests that mu type opioid receptors in the rat PAG are coupled to G-protein-mediated inhibition of adenylyl cyclase.
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PMID:Mu type opioid receptors in rat periaqueductal gray-enriched P2 membrane are coupled to G-protein-mediated inhibition of adenylyl cyclase. 254 57

The interaction with nitrous oxide analgesia of drugs that act at the benzodiazepine receptor was evaluated in the rat tail flick model. Nitrous oxide produced dose-related analgesia, which was potentiated by diazepam, a benzodiazepine agonist, antagonized by noreleagnine, a benzodiazepine inverse agonist. Pretreatment with the benzodiazepine antagonist Ro 15-1788 blocked the effects of both diazepam and noreleagnine on nitrous oxide analgesia. Subanesthetic doses of sodium pentobarbital and chloral hydrate produced nonsignificant trends to reduce the analgesic action of nitrous oxide. These data provide evidence for the presence of specific benzodiazepine receptors capable of modulating the analgesic effect of nitrous oxide.
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PMID:Modification of nitrous oxide analgesia by benzodiazepine receptors. 260 55

Preparations of local anesthetics are prepared as acidic solutions of the salts to promote solubility and stability. In solution, these salts exist as both nonionized and ionized forms. The ratio depends on the pH of the solution, and it is only the non-ionized form that permeates the nerve membrane and sheath. This study of epidural analgesia was undertaken to determine the effect of increasing the pH of the lidocaine HCl by the addition of sodium bicarbonate. Parameters studied included the time of onset of analgesia (time between the completion of injection and the loss of scratch sensation at the left L1 dermatome), the spread of sensory blockade, the degree of motor block, and the blood pressure and heart rate. Eighty seven adult patients undergoing epidural anesthesia were divided into four groups. Group 1 patients were given 2% lidocaine HCl solution plus 1.5 mL normal saline per 10 mL of lidocaine (pH 5.55). Group 2 patients were given 2% lidocaine HCl solution plus 1.5 mL 7% sodium bicarbonate per 10 mL of lidocaine (pH 7.04). Group 3 received 2% lidocaine HCl solution with 1:200000 epinephrine plus 1.5 mL normal saline per 10 mL of lidocaine (pH 5.68). Group 4 received 2% lidocaine HCl solution with 1:200000 epinephrine plus 1.5 mL 7% sodium bicarbonate per 10 mL of lidocaine (pH 7.11). The time of onset of analgesia and the spread of sensory blockade were more rapid in groups 2 and 4. The degree of motor block was more pronounced in these two groups, as were the changes in blood pressure and heart rate.
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PMID:[pH-adjusted lidocaine HCl with or without epinephrine for epidural anesthesia]. 260 12


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