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

In order to investigate the correlation between the peripheral ACh and the primary input of acupuncture sensation, in the paper the cholinesterase inhibitor--Neostigmine and the ACh synthesis blocker--Hemicholine, which are unable to pass through blood brain barrier, and ACh were used as tools to increase or decrease the level of ACh in peripheral nerve system of rats. The results indicated that: 1) The effect of electroacupuncture analgesia can be enhanced by subcutaneous injection of neostigmine which related to the dosage used. 2) The influence of electroacupuncture analgesia can be markedly inhibited by intraperitoneal injection of Hemicholine. 3) This influence of suppression by Hemicholine can be reversed at once when acetylcholine in combination with neostigmine was injected. But could not reverse by neostigmine alone. It suggested that the effect of electroacupuncture analgesia and the primary input of acupuncture sensation were significantly related to the level and content of ACh in periphery.
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PMID:[Acetylcholine and the primary input of acupuncture sensation--influence of peripheral acetylcholine on the role of electroacupuncture analgesia]. 212 63

The ability of acetylcholine muscarinic agonists, injected subcutaneously (s.c.) to elicit yawning and analgesia (tail-flick response) in rats was examined. Yawning was elicited by physostigmine, RS86 and pilocarpine with an inverted 'U'-shaped dose-response relationship; maximal effects occurred at 0.1, 0.5 and 2.0 mg/kg respectively. Neostigmine (0.05-0.2 mg/kg); arecoline (0.5-2.0 mg/kg); bethanecol (0.1-10 mg/kg) and McN-A-343 (5-20 mg/kg) had marginal or no activity. In contrast, dose-related analgesia was obtained following oxotremorine (0.01-0.3 mg/kg) and arecoline (0.5-4.0 mg/kg) and physostigmine (0.1-0.4 mg/kg), RS86 (0.25-2.5 mg/kg) and pilocarpine (0.5-8.0 mg/kg). The effects of acetylcholine antagonists on physostigmine-induced yawning and physostigmine-induced analgesia were also investigated. Following their s.c. injection, trihexyphenidyl, atropine, dicyclomine, secoverine and methylatropine but not pirenzepine, inhibited both yawning and analgesia; there were clear differences in their potencies on the two responses. Pirenzepine, intracerebroventricularly (i.c.v.), inhibited yawning (ED50 value 5.7 micrograms/rat) but not analgesia (3-100 micrograms/rat). The results are discussed in terms of a possible functional differentiation of central muscarinic receptors.
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PMID:Effects of acetylcholine agonists and antagonists on yawning and analgesia in the rat. 365 42

Rats were tested for tail-flick responses and then immediately subjected to footshock for 30 sec. This procedure induced analgesia, i.e. prolonged the latency of the tail-flick response, which was maximal immediately after the shock and decayed to normal levels within 2 hr. No analgesia occurred if either the analgesia test before the shock or the shock itself was omitted. The dependence of the analgesia on the association between the test before the shock plus the shock, suggests that this was a form of avoidance learning. The effects of drugs injected immediately after the shock were determined on latency of the tail-flick response, measured 2 hr later. Drugs known to improve memory, including physostigmine, pramiracetam and the muscarinic agonists, oxotremorine and RS 86, selectively induced analgesia in rats subjected to test before the shock plus the shock, thereby supporting a hypothesis of avoidance learning. Neostigmine and atropine methyl nitrate had no effect, indicating that the effects were mediated centrally. The learning effects were distinguishable from analgesia induced by drugs, since morphine increased analgesia regardless of the presence or absence of the test before shock or the shock. Also, naloxone, which had no effect per se, blocked analgesia induced by morphine but enhanced physostigmine-induced analgesia. Neither chlordiazepoxide nor D-amphetamine produced any changes in the latency of the tail-flick responses indicating that neither anxiolytic/muscle relaxant nor stimulant actions were involved.
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PMID:The effects of cholinergic drugs support an avoidance learning hypothesis of brief footshock-induced analgesia. 378 83

The influence of physostigmine was studied on the effect of morphine on the cardiovascular and respiratory systems in conscious rabbits. Morphine (4 mg/kg i.v.) caused analgesia, bradycardia, hypotension and respiratory depression, as indicated by a fall in respiratory rate of 50%, a rise in blood PaCO2 from 25.1 to 37.2 mm Hg and a fall in pH from 7.40 to 7.24. These effects lasted 2 to 3 hr and were completely antagonized by naloxone. Physostigmine (2.5 or 5 microgram/kg/min) given by constant i.v. infusion did not significantly alter blood pressure or heart rate, but decreased blood PaCO2 from 25.1 to 19 mm Hg and increased pH from 7.40 to 7.46. Pretreatment of rabbits with physostigmine (5 microgram/kg/min) completely prevented both the fall in blood pressure and blood pH and the rise in PaCO2 induced by morphine (4 mg/kg) and also significantly reduced both the intensity and duration of bradycardia. Analgesics activity of morphine remained unimpaired by physostigmine. Neostigmine (2.5 microgram/kg/min) potentiated the bradycardia induced by morphine and did not antagonize its hypotensive and respiratory depressant effects. The results support the hypothesis that the respiratory and cardiovascular depressant effects of morphine, but not the analgesia, results from an inhibition of acetylcholine release from neurons in the central nervous system.
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PMID:Antagonism of the cardiovascular and respiratory depressant effects of morphine in the conscious rabbit by physostigmine. 725 49

The ability of physostigmine to antagonize the respiratory depressant effect of morphine was studied in conscious rabbits and ketamine-anaesthetized dogs pretreated with atropine methyl nitrate. Morphine 4 mg kg-1 increased PaCO2 in the rabbit from 3.43 +/- 0.16 to 4.95 +/- 0.28 kPa, decreased arterial pH from 7.45 +/- 0.01 to 7.31 +/- 0.01 and decreased respiratory frequency by 36%. Physostigmine 0.1 mg kg-1 reduced PaCO2 to control values within 10 min and significantly increased arterial pH and respiratory frequency. There was no antagonism of the analgesic effect of morphine. Neostigmine 0.1 mg kg-1 did not reverse the respiratory depressant effect of morphine. In dogs anaesthetized with ketamine, morphine 15 mg kg-1 caused loss of consciousness and marked analgesia, decreased the respiratory frequency by 47%, and increased PaCO2 by 47%. Physostigmine 0.1 mg kg-1 antagonized the effect of morphine on respiration and restored consciousness in the dogs, but did not impair analgesia. It is concluded that physostigmine reverses morphine-induced respiratory depression by prolonging the effect of acetylcholine released from brain-stem neurones. The possibility should be considered of replacing opiate antagonists by physostigmine to reverse postoperative respiratory depression and drowsiness induced by opiates.
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PMID:Physostigmine antagonizes morphine-induced respiratory depression but not analgesia in dogs and rabbits. 744 96

In modern anaesthesia various antagonists are used. They provide efficient tools to facilitate better control of pharmacological effects and side effects of drugs routinely used in anaesthesia. Naloxone is a competitive antagonist of opioids without any intrinsic activity. It counteracts respiratory depression, pruritus, sedation and analgesia caused by opioids. It is fast-acting with a duration of action of 45 to 90 min. Several investigators have reported severe side effects of naloxone including hypertension, tachyarrhythmias, left heart failure and cardiac arrest, and hence the use of naloxone must be carefully considered in every single patient. Flumazenil is a competitive antagonist of benzodiazepines. It is a remarkably safe drug and very effective to terminate all benzodiazepine effects in anaesthesia and intensive-care patients. Serious complications caused by flumazenil have been reported in patients receiving benzodiazepines in the treatment of seizure disorders and in patients with mixed intoxications. Neostigmine is one of several antagonists of neuromuscular blocking agents. Its side effects include bradycardia, increased bronchial secretions and increased peristalsis. Indication depends on the results of neuromuscular monitoring. Physostigmine is an unspecific antagonist of the central anticholinergic syndrome, an acute psychosis that may be caused by numerous drugs used in anaesthesia. Generally, antagonists should be carefully titrated. In emergency medicine the use of these antagonists is not recommended; the primary goal is to restore vital functions.
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PMID:[Antagonists in anesthesia]. 854 33

Two patients suffering with severe pain due to metastatic abdominal neoplasm were selected to examine whether subarachnoid neostigmine provided effective pain relief. Neostigmine was injected through a catheter introduced into the subarachnoid space at L4-L5. Patients were monitored for changes in arterial blood pressure, cardiac and respiratory rates, body temperature, level of consciousness and neurologic change. Pain was classified by the patients on a verbal four-grade scale, and analgesia was classified on a verbal three-grade scale. Complete pain relief was obtained 2 h after neostigmine (0.2 mg) in one patient and 4 h after neostigmine (0.1 mg) in the second patient. Pain of mild intensity returned 20 and 22 h after drug administration, respectively. Gastrointestinal discomfort was observed in both cases, but nausea and vomiting occurred only in the patient treated with the highest dose of neostigmine. No significant change in the monitored parameters was observed, except for a 6-h period of decreased blood pressure in the patient treated with the lower dose of neostigmine which required no specific treatment. The results obtained in these anecdotal cases indicate that subarachnoid neostigmine may provide analgesia in patients with pain arising from neoplasia, but further studies using controlled trials are needed before the drug is brought into clinical use.
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PMID:Analgesic effect of subarachnoid neostigmine in two patients with cancer pain. 888 Aug 64

Spinal neostigmine causes analgesia in animals and humans and abolishes hypotension from spinal bupivacaine in rats. Since drug distribution and action can vary with the size of the spinal cord, we tested the effects of the maximum tolerated dose of spinal neostigmine alone and with bupivacaine in conscious sheep. Neostigmine alone increased arterial blood pressure by 10%, with a statistically significant increase beginning 30 min after injection. Compared with spinal bupivacaine alone, addition of neostigmine resulted in hypotension of slower onset (15 vs 5 min), shorter duration (45 vs 105 min), and smaller magnitude (-18% +/- 3% vs -37% +/- 6%). Addition of neostigmine did not affect height of sensory block from spinal bupivacaine. These data agree with preliminary clinical reports that spinal neostigmine diminishes, but does not abolish, hypotension from spinal bupivacaine in humans.
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PMID:Spinal neostigmine diminishes, but does not abolish, hypotension from spinal bupivacaine in sheep. 889 82

Intrathecal (IT) neostigmine produces analgesia in animals and humans and enhances systemic opioid analgesia. To examine the safety of IT neostigmine for eventual use in obstetrics, we studied 24 healthy, term pregnant patients scheduled to receive elective cesarean section using a combined spinal-epidural anesthetic. Using an open-label, dose-ranging design, patients received either IT placebo or neostigmine 10, 30, or 100 microg in a 1-mL solution of 5% glucose in normal saline followed in 15 min by 2% epidural lidocaine for cesarean section. Neostigmine did not affect fetal heart rate tracings or Apgar scores. The women received patient-controlled analgesia intravenous morphine postoperatively. Compared with the glucose control, neostigmine produced a dose-independent reduction in postoperative morphine use. Cumulative average 24-h morphine use was 82 +/- 7 mg for women receiving IT placebo and 50 +/- 8 mg for women receiving IT neostigmine (P < 0.003). Hourly morphine use was significantly reduced in the neostigmine groups for 10 h postoperatively. These data indicate that IT neostigmine can produce 10 h of post-cesarean section analgesia without adverse fetal effects and support cautious further prospective study.
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PMID:Intrathecal neostigmine for post-cesarean section analgesia: dose response. 917 5

Intravenous opioids cause analgesia and increase release of ACh in spinal cord dorsal horn in animals, and these effects are enhanced by intrathecal neostigmine injection. The purpose of the current study was to test whether intrathecal neostigmine enhanced analgesia and increased cerebrospinal fluid concentrations of ACh over those induced by i.v. alfentanil in volunteers, and also to test whether neostigmine enhanced alfentanil-induced side effects. After human studies committee approval, 40 healthy volunteers received an intrathecal injection of saline or neostigmine (50, 100 or 200 microg) followed in 60 min by a computer-controlled, stepped i.v. infusion of alfentanil to escalating targeted plasma concentrations. Pain report to hand and foot immersion in ice water, sedation, nausea, weakness, vital signs, end-tidal CO2 and oxyhemoglobin saturation were measured 60 min after spinal injection and at the end of each 20-min alfentanil infusion. Cerebrospinal fluid was sampled once after drug administration. Intrathecal neostigmine alone caused analgesia in the foot but not in the hand, and was accompanied by leg weakness, whereas IV alfentanil alone caused equivalent analgesia in both the hand and the foot and was accompanied by nausea, sedation, increased end-tidal CO2 and decreased oxyhemoglobin saturation. Neostigmine enhanced analgesia but not respiratory effects induced by i.v. alfentanil; it also enhanced nausea and sedation. Intravenous alfentanil increased cerebrospinal fluid ACh concentration, and neostigmine enhanced this change. These data in humans are consistent with a spinal cholinergic mechanism of i.v. opioid analgesia. Because neostigmine enhances both analgesia and side effects induced by i.v. alfentanil, the clinical utility of their use in combination will depend on the relative strength of these interactions.
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PMID:Enhancement of analgesia from systemic opioid in humans by spinal cholinesterase inhibition. 922 43


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