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 onset, quality and duration of analgesia following extradural pethidine 50 mg and i.m. pethidine 100 mg was assessed in 30 postoperative patients who had undergone Caesarean section under extradural anaesthesia. Saline and pethidine were given in a randomized, double-blind fashion using simultaneous extradural and i.m. injections. Extradural pethidine provided superior analgesia, of quicker onset but similar duration, and both treatments were associated with a low incidence of side effects.
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PMID:Analgesia following extradural and i.m. pethidine in post-caesarean section patients. 210 96

Angiotensin II (AII), arginine vasopressin (AVP) and prolactin (PRL) were measured by radioimmunoassay in plasma and cerebrospinal fluid (CSF) in concurrent daily samples from conscious unrestrained steers. Packed cell volume, [Na+] and osmolality were also measured from these samples. Salt appetite was assessed during a 5-min daily session of operant conditioning. Food and water was always available. Unilateral parotid duct fistulation was effected under xylazine analgesia and halothane/O2 anaesthesia. To prevent a sodium deficit developing from loss of [Na+] in the extruded saliva, 0.3 M NaHCO3 was available ad libitum so that each animal could ingest sufficiently to balance the salivary loss. A week later epidural cannulae were implanted in the cisternae magna using the same anaesthesia. Three days afterwards when the saliva [Na] was 78 mmol/1, the 0.3-M NaHCO3 supplement was withdrawn for 7 days so that sodium deficiency developed to a degree which evoked salt appetite. When the NaHCO3 supplement was restored ad libitum, all aspects of [Na+] deficiency and salt appetite were completely ameliorated within 2-3 days. Packed cell volume increased and body weight decreased (p less than 0.05) during depletion, but rapidly returned to normal on day 2 of repletion. Both plasma and CSF osmolality were reduced during depletion as were plasma [Na+] (p less than 0.01) and CSF [Na+] (p less than 0.001). From a basal value of 64.7 +/- 9.35 fmol/ml on day 0, plasma AII increased to 229.2 +/- 46.65 fmol/ml (p less than 0.001) on day 3, prior to the onset of salt appetite on days 4-7. In marked contrast to plasma AII during sodium depletion, CSF AII was unchanged during salt appetite. There was no correlation between plasma and CSF AII during behavioural salt appetite.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of endogenous systemic and brain angiotensin II, arginine vasopressin and prolactin with the genesis of salt appetite in cattle. 284 67

In order to determine the behavioral characteristics of the neonatal opioid system during distressful situations, a modification of the hot-plate paw-lick test used on adults was developed for infant rats. Ten-day-old pups were analgesic to heat following morphine administration. Pretreatment with an opioid antagonist prevented the analgesia. Morphine analgesia was significantly greater in pups group isolated from the dam. Saline control pups group isolated from the dam exhibited longer latencies than their nest-housed siblings. Individual isolation for 5 min increased paw-withdrawal latency markedly. This was also naltrexone reversible. This analgesia was not seen when pups were tested directly from the nest or when grouped with other pups for the 5 min. It is suggested that the opioid system(s) for stress and pain are functional in Day 10 rats and short-term isolation from the dam is a probable natural stressor that is modulated by endogenous opioid release.
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PMID:Behaviorally functional opioid systems in infant rats: II. Evidence for pharmacological, physiological, and psychological mediation of pain and stress. 364 Jun 42

Naloxone blockade of stimulation-produced analgesia in the rat is partial and variable. In the present study the effectiveness of the long-acting narcotic antagonist naltrexone is examined. Bipolar stainless steel electrodes were implanted in the dorsal raphe nucleus or ventral periaqueductal gray matter of male rats. Analgesia produced by electrical stimulation was tested by the tail flick method before and twenty min following the administration of saline or naltrexone. Saline administered IP failed to alter the analgesic response. Following naltrexone the degree of analgesia was reduced by a mean of 79% for IV injection (3.7 mg/kg) and by means of 26%, 52%, 81% and 83% for IP administration of 0.3, 1.0, 3.0 and 10 mg/kg, respectively. These results confirm the participation of opiate mechanisms in stimulation-produced analgesia, and indicate that, under certain circumstances, only opiate mechanisms are involved.
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PMID:Blockade by naltrexone of analgesia produced by stimulation of the dorsal raphe nucleus. 729 Dec 46

The analgesic effects of the non-steroidal anti-inflammatory drugs (NSAIDs) flunixin and dipyrone were assessed in healthy sheep with no pre-existing inflammation, and in sheep with a chronic inflammatory lesion, using a mechanical noxious stimulus. Saline and dexamethasone were given as controls. Blood taken from healthy sheep after NSAID administration was assayed for thromboxane B2 (TxB2) to compare the ability of these drugs to inhibit cyclo-oxygenase. Both flunixin and dipyrone produced a small but statistically significant rise in pain thresholds (18% and 21% of maximum possible effect respectively) in the healthy sheep which peaked at 30 min and had returned to pre-drug values by 2-3 h. In the lame sheep a similar effect occurred but the response was smaller, much more variable and tended to be prolonged. Saline and dexamethasone had no effect on thresholds over 6 h in either group of sheep. The rise in thresholds was prevented by pre-treatment with naloxone (an opioid antagonist) or atipamezole (an alpha 2-adrenergic antagonist) in the healthy sheep. Naloxone and atipamezole had no effect on thresholds when given alone to healthy sheep. Both NSAIDs inhibited the production of TxB2 to a similar extent. These results indicate that central mechanisms may be involved in NSAID analgesia.
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PMID:The effects of opioid and alpha 2 adrenergic blockade on non-steroidal anti-inflammatory drug analgesia in sheep. 767 50

Ropivacaine, a new long-acting amino-amide local anaesthetic agent, and bupivacaine, in various concentrations with or without addition of adrenaline, were tested in a randomized, double-blind study using intradermal wheals. Ten non-smoking, healthy, young male volunteers participated. In series I plain solutions of ropivacaine (0.25%, 0.5%, 0.75% and 1%) and bupivacaine (0.25%, 0.5% and 0.75%) were injected intradermally and in series II the same concentrations, with the addition of adrenaline 5 ug.ml-1 (1:200,000), were used. The same volunteers took part in both series, with an interval of at least three weeks between the experiments. Saline was included as control in both series. Pin-pricking was used to assess the dermal analgesia. Plain solutions of ropivacaine produced significantly longer durations of dermal analgesia than did plain solutions of bupivacaine, in all tested concentrations. A significant increase in duration was seen for both local anaesthetics when adding adrenaline. Local vascular effects at the injected areas were determined by visual inspection (nil, pink, pale). Local blanching (pale) was significantly more frequent for plain solutions of ropivacaine, in all tested concentrations. Local redness (pink) was significantly more frequent with plain bupivacaine, in a dose-dependent relation. An initial redness was frequently observed for both local anaesthetics containing adrenaline, followed by blanching at most sites.
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PMID:Local analgesic and vascular effects of intradermal ropivacaine and bupivacaine in various concentrations with and without addition of adrenaline in man. 806 17

1. A cross-over single blind study examined the possible central effects of non-opioid analgesic drugs on the trigeminal reflexes. 2. The corneal reflex and blink reflex (R1, R2) were recorded electromyographically and response areas measured in healthy volunteers before and after intramuscular injection of piroxicam (40 mg); and after intravenous injection of lysine acetylsalicylate (500 mg). After the last drug recording the subjects received intravenous naloxone (2 mg) followed 5 minutes later by further reflex testing. Saline was used as a placebo in control experiments. 3. Both analgesics reduced the corneal reflex: piroxicam induced a 27% and lysine acetylsalicylate a 21% a reduction that naloxone did not reverse. Neither drug reduced the early or the late component of the blink reflex. 4. The marked inhibitory changes that the two non-narcotic analgesics produced on the corneal reflex--a nociceptive response--indicate a centrally-mediated action. 5. Naloxone's failure to reverse the induced analgesia argues against opiate receptor mediation.
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PMID:Analgesic-antiinflammatory drugs inhibit orbicularis oculi reflexes in humans via a central mode of action. 811 66

We have examined the efficacy, duration of action and side effects of extradural diamorphine alone and in combination with 1:200,000 adrenaline in a randomized, double-blind controlled study of 45 patients who underwent Caesarean section under spinal anaesthesia. Saline 10 ml, diamorphine 2.5 mg in saline 10 ml or diamorphine 2.5 mg in 1:200,000 adrenaline 10 ml were administered via the extradural route at delivery of the baby. Both diamorphine and diamorphine with adrenaline provided significantly prolonged analgesia compared with control (mean time to next analgesia (95% confidence interval) 17.3 h (12.0, 22.1 h), 15.9 h (10.6, 21.1 h), 5.7 h (1.5, 9.9 h), respectively) (P < 0.01). The addition of adrenaline increased the quality of analgesia 8 h after operation, but had no effect on the total amount of i.m. morphine administered during the first 24 h. The incidence of side effects was similar in all groups.
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PMID:Effect of extradural diamorphine on analgesia after caesarean section under subarachnoid block. 828 May 44

We have recently reported that a short-acting anesthetic and analgesic drug midazolam can produce analgesia and decrease morphine tolerance and dependence in the rat by interacting with the opioid system. This study was designed to investigate the effect of midazolam, morphine, and both together on beta-endorphin levels in the rat. Male Sprague-Dawley rats were divided into four groups: (1) saline-saline; (2) saline-morphine; (3) midazolam-saline, and (4) midazolam-morphine groups. First, saline or midazolam injection was given IP and after 30 min a second injection of saline or morphine was given subcutaneously once daily for 11 days. Animals were sacrificed on 11th day 60 min after the last injection, to measure beta-endorphin by radioimmunoassay. Saline-morphine-treated animals showed a significant increase in beta-endorphin levels in the cortex, pons, medulla, lumbar spinal cord, adrenals, and spleen, and a decrease only in its level in pituitary. Midazolam-saline-treated animals showed a significant increase in beta-endorphin levels only in the medulla, and a decrease in its levels in hippocampus, striatum, and adrenals. Saline-morphine-treated animals did not show any changes in plasma beta-endorphin, but animals treated with midazolam-saline had a significant decrease in plasma beta-endorphin. In rats treated with morphine and midazolam together, beta-endorphin levels in cortex, lumbar spinal cord, and spleen decreased to the similar levels observed in rats treated with saline-saline; in pons and cervical spinal cord the levels were even lower than that found in saline-saline group. The decrease in pituitary beta-endorphin in morphine-midazolam-treated rats was due to morphine's own activity, whereas the decrease in plasma beta-endorphin in hippocampus in the morphine-midazolam group was a synergistic effect of morphine and midazolam. The beta-endorphin level in adrenal glands in the morphine-midazolam-treated animals was not different from that found in rats treated with morphine alone but was still higher than that in the saline-saline group. In general, it appears that chronic treatment with morphine stimulates the beta-endorphinergic system. A concomitant treatment with midazolam abolishes the stimulatory effect of morphine on the beta-endorphinergic system. These results may help us in understanding the intrinsic mechanisms involved in narcotic tolerance and dependence.
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PMID:Effect of chronic treatment with morphine, midazolam, and both together on beta-endorphin levels in the rat. 897 37

Fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), significantly potentiates analgesia when administered in animals together with opioids. The aim of the present study was to investigate the effects of fluvoxamine on sufentanil antinociception and tolerance. Following animal care committee approval, the effects of continuous infusions of fluvoxamine and sufentanil were studied in behavioural tests (hot-plate test, tail-flick test, catalepsy test) in Sprague-Dawley rats with a jugular vein catheter. Saline was administered as a control. The time-effect curves for continuous intravenous sufentanil indicate dose-related antinociception and rapid development of tolerance in the hot-plate and tail-flick tests. Co-administration of fluvoxamine with continuous sufentanil enhances antinociception and attenuates development of tolerance, most clearly seen in the tail-flick test. Fluvoxamine alone and saline were not effective. No animal showed catalepsy. As a side effect we observed a marked loss of body weight. The IC50 values of sufentanil binding with and without fluvoxamine addition are 0.56+/-0.17 nM and 0.3+/-0.15 nM, respectively, indicating no direct effect on the occupancy of sufentanil on the mu-receptor by this serotonin reuptake inhibitor. In conclusion, we were able to show that the combination of an opioid with an SSRI at low doses improves analgesia and decreases development of tolerance in nociceptive tests in rats. The clinical implications of these promising results in an animal model, however, await further investigation.
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PMID:Effect of fluvoxamine on sufentanil antinociception and tolerance under chronic intravenous infusion in rats. 1062 1


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