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

Parturients in whom meperidine HCl, propiomazine HCl, and scopolamine were used for analgesia and amnesia in labor and delivery were studied to determine the efficacy and safety of physostigmine reversal after delivery. Of a total of 120 patients, 108 received physostigmine salicylate at the completion of episiotomy closure, awakening in an average of 7.5 minutes compared with 137.8 in 12 controls. Physostigmine appears to be a safe, rapidly effective agent for reversing the prolonged somnolence of this sedation regimen.
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PMID:Physostigmine reversal of sedation in parturients. 0 75

The effects of centrally acting agents which alter cholinergic activity were assessed in mice rendered tolerant to and dependent on morphine (M mice) and in naive mice (N mice). In both N and M mice, physostigmine potentiated morphine analgesia slightly, and this action was blocked by atropine and scopolamine. When administered 10 min before naloxone in dependent mice atropine enhanced precipitated withdrawal jumping; when given 30 min before naloxone, atropine produced an inhibition of the response. Physostigmine abd oxotremorine greatly inhibited the jumping response, while echothiophate had no effect. The inhibitory effect of physostigmine on naloxone precipitated withdrawal jumpimg was reversed by atropine and scopolamine but atropine did not alter morphine tolerance and dependence development. Brain acetylcholine (ACh) levels in both N and M mice were increased by physostigmine, the increase being greater in M mice. This increase was blocked by prior administration of atropine or scopolamine. When atropine was administered to M mice 10 min before sacrifice, brain AC-h levels decreased. However, when brain ACh levels were determined 30 min after atropine, no change was found. It was concluded that ACh does not play a major direct role in the development of tolerance and dependence, but that ACh is involved in the manifestations of acute morphine effects and in some of the withdrawal signs in the dependent state.
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PMID:Morphine tolerance and physical dependence: influence of cholinergic agonists and antagonists. 94 35

This study compared the effects of 3 novel antiAChE agents (derivatives of dimethylaminoethyl-phenyl carbamate) with that of physostigmine on the respiratory depression induced by morphine in rabbits. Each drug, RA6, (1 mg i.v., 2 mg s.c.) RA7 (1 or 2 mg i.v.); RA15 (0.25 or 0.5 mg i.v.), physostigmine (0.05 or 0.1 mg i.v.) or saline (1 ml), was injected simultaneously with morphine (8 mg i.v.) to groups of 6-10 rabbits. Respiration rate, blood gases and pH were monitored for 3 hr. Plasma ChE was measured before and at 15 min intervals after injection. The 4 antiAChE's were given to 40 other rabbits, which were sacrificed at the time of maximal antagonism of the respiratory depressant effect of morphine, in order to measure the activity of AChE in the medulla, cortex and hippocampus. Physostigmine (0.1 mg) only antagonized the increase in paCO2 induced by morphine at 15 and 30 min. The drugs RA15 (0.5 mg), RA6 (2.5 mg) and RA7 (2 mg) almost completely prevented the respiratory depression, without obvious signs of peripheral cholinergic hyperactivity, for at least 3 hr. There was no relationship between the degree of antagonism of the effects of morphine with any drug and that of inhibition of ChE in plasma. In contrast, a highly significant correlation (P less than 0.01) was found between the former and the amount of inhibition of AChE in the medulla. It is suggested that the novel carbamates may have potential therapeutic application in reducing the respiratory depression of opiates, without impairing analgesia.
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PMID:Antagonism of morphine-induced respiratory depression by novel anticholinesterase agents. 175 86

Effects of physostigmine on ketamine-induced anesthesia and analgesia were studied in male Sprague-Dawley rats using behavioral tests. Rats were divided into six groups. Immediately after loss of the righting reflex following an intraperitoneal injection of ketamine 75 mg/kg, each group of rats was given an intraperitoneal injection of either physostigmine 0.05, 0.1, 0.2, 0.4, 0.6 mg/kg or saline as the control, respectively. Physostigmine 0.1 mg/kg caused the greatest antagonistic effect on ketamine anesthesia as indicated by sleeping time, duration of ataxia and motor coordination. The antagonistic effects of physostigmine were reduced by a dose of physostigmine of greater than 0.1 mg/kg. However, at no dose did physostigmine antagonize ketamine analgesia as indicated by the tail-flick latency. Physostigmine (0.4 and 0.6 mg/kg) itself had analgesic and motor-suppressive actions. It can therefore be presumed that there is a limited threshold of the dose of physostigmine which develops an antagonistic effect on ketamine anesthesia due to the motor-suppressive action. It is also confirmed that physostigmine itself produces analgesia, and does not antagonize ketamine-induced analgesia.
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PMID:Antagonistic effect of physostigmine on ketamine-induced anesthesia. 225 36

In order to antagonize immediate postoperative somnolence, 24 surgical patients were given a two-rate infusion of physostigmine, aiming at a constant plasma concentration in the range of 1 to 10 ng/ml. Plasma concentrations of physostigmine were determined during infusion and after infusion and the effects of physostigmine on analgesia and postoperative sedation, and its side effects were monitored throughout. On the 1st postoperative day some of the patients (n = 8) were given 5 mg physostigmine orally, after which plasma concentrations as well as effects were measured. Steady-state concentrations were generally lower than predicted. Clearance varied between 10 and 85 ml/min x kg with a mean of 40.8 +/- 21.0 ml/min x kg. Oral bioavailability was 25.3 +/- 11.1%. Physostigmine administered as an intravenous infusion antagonized immediate postoperative somnolence in 21 out of 24 patients. Effects were poorly correlated with the established steady-state concentration of physostigmine. The patients' experience of postoperative pain relief was mostly satisfactory and the side effects of physostigmine infusion were generally limited. The effects of physostigmine in the immediate postoperative period seemed dependent on the dose as well as on the time which had elapsed since administration of anticholinergic drugs. After oral physostigmine administration the following morning, the majority of patients experienced side effects such as nausea and abdominal pain. In conclusion, physostigmine given as infusion antagonizes postoperative somnolence. However, the arousal effect was considered not better than that resulting from a bolus dose of the drug, although the infusion regimen allowed a prolonged clinical effect duration.
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PMID:Reversal of postoperative somnolence using a two-rate infusion of physostigmine. 258

1. Baclofen induced analgesia was confirmed by means of the mouse hot plate test. 2. Physostigmine significantly increased the response to baclofen whilst neostigmine was ineffective. Baclofen analgesia was reduced by atropine. 3. The response to baclofen was increased by the administration of tolazoline, propranolol and nadolol. In contrast, the analgesic response to morphine was attenuated by the antiadrenergic drugs phenoxybenzamine, tolazoline and nadolol.
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PMID:Influence of adrenergic and cholinergic mechanisms in baclofen induced analgesia. 334 2

Despite the widespread use of meperidine as an analgesic, its potential for producing delirium has been overlooked. Six cases demonstrating meperidine-induced behavioral toxicity are reported. Toxicity was more likely when meperidine was combined with cimetidine or drugs having anticholinergic activity. Discontinuation of meperidine and substitution of morphine for analgesia were usually successful in treating the delirium. Physostigmine reversed the delirium in one patient. The authors suggest that the delirium results from the excessive anticholinergic activity of meperidine or its only active metabolite, normeperidine.
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PMID:Meperidine-induced delirium. 360 28

A clinical trial of the combination of naloxone in a low dose (1-1.5 micrograms X kg-1 body weight) with physostigmine (0.5-1.0 mg i.v.) was made to elucidate whether this combination could reverse postanaesthetic overdosing in neurosurgical patients without increasing postoperative pain. The investigation was made following previous findings that physostigmine has analgesic properties in addition to its systemic antisedative and anticholinergic effects as well as a stimulatory effect on morphine-depressed ventilation. Altogether 198 neurosurgical patients were investigated. The results showed that postanaesthetic over-sedation can be safely treated by a combination of naloxone and physostigmine in the dosages named above, resulting in the rapid reversal of sedation, where opiates, neuroleptics and benzodiazepines have been used. In contrast, this combination has very little effect on sedation following the administration of agents such as halothane and isoflurane. In the great majority of patients (95%), the treatment resulted in excellent analgesia during the first postoperative hour. The incidence of nausea and vomiting was increased somewhat by this treatment, but these side-effects could be minimized by decreasing the rate of drug administration. Physostigmine is contra-indicated in patients having symptoms and signs similar to those of Parkinson's disease, and the dose of physostigmine should also be reduced to 0.5 mg i.v. in all patients over the age of 65.
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PMID:Reversal of sedation and respiratory depression after anaesthesia by the combined use of physostigmine and naloxone in neurosurgical patients. 376 92

Two case reports are presented of patients with post-thoracotomy pain treated with epidural morphine who developed somnolence several hours after the procedure. Physostigmine, 1 mg IV successfully reversed the somnolence without any effect on analgesia.
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PMID:The reversal of epidural morphine induced somnolence with physostigmine. 649 85

This study concerns the cholinergic involvement in three experimental procedures which produce analgesia. Rats were given one of seven treatments: saline (1.0 ml/kg, i.p.); morphine sulfate (3.5, 6.0 or 9.0 mg/kg, i.p.); physostigmine salicylate (0.65 mg/kg, i.p.); warm water swim (3.5 min at 28 degrees C); and cold water swim (3.5 min at 2 degrees C). Each rat was tested on a hot plate (59.1 degrees C) once prior to and 30 min after treatment. Immediately after the last test the rats were killed with focussed microwave radiation. Levels of acetylcholine (ACh) and choline (Ch) in six brain areas (brain stem, cerebral cortex, hippocampus, midbrain, cerebellum and striatum) were analyzed by gas chromatograph-mass spectrometer. Morphine (9.0 mg/kg), physostigmine and cold water swimming caused significant analgesia. Morphine elevated the levels of ACh in the cerebellum and striatum, cold water swimming--in the cerebellum, striatum and cortex, and physostigmine--in the striatum and hippocampus. Levels of choline were elevated by morphine in the cerebellum, cortex and hippocampus, while cold water swimming elevated levels of choline in the cerebellum, cortex, striatum and hippocampus. Physostigmine did not change levels of choline in any of the brain areas studied. These data suggest that the analgetic effects of morphine or cold water swimming may be mediated by components of the cholinergic system that differ from those involved in the analgetic effects of physostigmine.
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PMID:Cholinergic mechanisms of analgesia produced by physostigmine, morphine and cold water swimming. 662 12


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