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

Hexacarbon compounds are neurotoxic to man and animals. These substances also inhibit various enzymes in vitro, including acetylcholinesterase. Since some cholinesterase inhibitors alter nociception we determined the effect of acute ip administration of 2,5-hexanedione on nociception in female Wistar rats (75-90 days old, 170-200 g; 15-17 rats in each group) using a tail-flick apparatus. The rats were injected ip with vehicle solution (120 mM NaCl containing 10 mM potassium phosphate buffer, pH 7.2) and 200, 400 or 800 mg/kg of 2,5-hexanedione in a volume of 1 ml/kg body weight. Tail-flick latencies were obtained 10, 30, 60 and 90 min after drug administration. All doses of 2,5-hexanedione caused antinociception (P less than 0.001) but the appearance and duration of the analgesia varied according to the dose of the drug. The highest dose tested (800 mg/kg) caused analgesia from 10 to 60 min, 400 mg/kg caused analgesia at 30 and 60 min, and 200 mg/kg produced antinociception only at 60 min after drug injection (P less than 0.05 for all the above comparisons). These results suggest that 2,5-hexanedione induces antinociception in rats. Whether this effect is mediated by a cholinergic mechanism is under investigation.
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PMID:Effect of acute administration of 2,5-hexanedione on nociception in rats. 179 54

In this study, male Sprague-Dawley rats (150-230 g), maintained under controlled lighting and temperature conditions, were used. In one experiment, glucose administration (10 g/kg) was found to be associated with profound analgesia which could be blocked by prior administration of atropine (0.5 mg/kg). In another experiment, when two doses of glucose were given at 24 hr interval, the second injection of glucose was associated with tolerance to glucose-induced analgesia. In an attempt to correlate changes in the cholinergic enzymes with glucose-induced analgesia, choline acetyltransferase and acetylcholinesterase activities were determined in the cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata in control rats and rats treated with a single dose of glucose (10 g/kg) or two doses of glucose. The second administration of glucose was accompanied with tolerance in the level of acetylcholinesterase in the bulbus olfactorius, midbrain, cerebral cortex, cerebellum and pons. There were no significant changes in choline acetyltransferase activities between the groups studied. The results obtained indicate that the cholinergic system may be involved in glucose-induced analgesia and that the rapid development of tolerance to glucose-induced analgesia is associated with the tolerance in the response of brain acetylcholinesterase activity.
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PMID:Involvement of the brain cholinergic system in the rapid development of tolerance to glucose-induced analgesia. 207 47

In this paper a preliminary study was made about the relationship between ACh and the primary input of acupuncture sensation based on the changes of content of ACh, its synthetic enzyme (choline acetylase, or ChAC) and its degradation enzyme (acetylcholinesterase, or AChE) in the dorsal horn of the spinal cord and spinal ganglia. The results were found that: 1) EA at "huantiao" exerted a marked analgesia effect, the acupuncture analgesia was inhibited when the lateral dorsal root was cut off. 2) The content of ACh of the EA group were slightly lower than those of the control group. 3) AChE activity in the spinal ganglia and the dorsal horn increased markedly under electroacupuncture stimulation. 4) The activity of ChAC in the dorsal horn of rats under acupuncture stimulation was significantly higher than those of the control group. 5) ACh content in the spinal ganglia increased obviously when the degradation of peripheral ACh was inhibited by prostigmine. 6) With the lumber dorsal roots excised, AChE activity of the operative side were much lower than those of the intact side during EA stimulation. It suggest that the metabolism of ACh in the dorsal horn of the spinal cord and spinal ganglia change during the course of EAA, and only when signals produced at the acupoints are delivered to the spinal cord via ACh-containing primary somatosensory nerves, can they exert analgesic and therapeutic effect of acupuncture.
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PMID:[The change of ACh metabolism in the dorsal horn of spinal cord and spinal ganglia during electroacupuncture analgesia (EAA)]. 211

The choline analog, N-amino-N,N-dimethylaminoethanol (NADe), was fed ad libitum (chloride salt; 0.5%) to weanling rats in a low choline, low methionine synthetic diet. Control rats were fed choline chloride (0.5%) in place of NADe. Initial observation and behavioral screen tests of grasp strength, startle reflex, righting reflex, analgesia (hot plate test) and body temperature did not reveal any toxic effects caused by NADe, although both experimental and control groups gained weight more slowly than rats fed standard lab chow. After 25 days on the diet, the performance of rats fed NADe in a one-trial passive avoidance test was significantly impaired compared to control rats. There was no difference between experimental and control rats in sensitivity to foot shock or in activity monitored in a closed field. A subjective, 6-component behavioral rating scale indicated rats fed NADe were resistant to handling but not aggressive. These behavioral results were similar in two separate feeding experiments using deuterium-labeled and unlabeled NADe. The twitch response of isolated rat phrenic nerve-diaphragms during stimulation did not show any impairment of neuromuscular function in rats fed NADe. Receptor binding experiments indicated there were no differences between experimental and control rats in tritiated quinuclidinyl benzilate [( 3H]QNB) binding capacity in cortex, heart and ileum. Competitive [3H]QNB binding with carbachol indicated there was no difference in the IC50's measured in cortex homogenates. Acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities in cortex were similar in experimental and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of chronic dietary administration of the cholinergic false precursor N-amino-N,N-dimethylaminoethanol on behavior and cholinergic parameters in rats. 301 61

An oedematous pre-eclamptic patient received lumbar epidural analgesia during labour. Clear fluid leaked from the skin puncture site for 4 days. The fluid was analysed using protein electrophoresis for cholinesterase enzymes and was found not to contain the cerebrospinal fluid specific form of the enzyme, acetylcholinesterase. The sensitivity of this test was explored using serial dilutions of cerebrospinal fluid. It is now possible to say that the leaking fluid did not contain cerebrospinal fluid.
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PMID:Acetylcholinesterase--a specific marker for cerebrospinal fluid. 337 51

In this study, male Sprague-Dawley rats maintained under controlled environmental conditions were used. Choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were determined in cerebral cortex, bulbus olfactorius, midbrain, hypothalamus, hippocampus, cerebellum, pons and medulla oblongata in control rats and rats treated with morphine (10 mg/kg) for 1 or 2 days. Repeated administration of morphine was associated with a decline in the degree of analgesia produced. Significant increase (p less than 0.01) in AChE activity of the medulla oblongata was observed following morphine administration for 1 or 2 days. A single injection of morphine resulted in a significant decline (p less than 0.01) in ChAT activity of hypothalamus, cerebellum and medulla oblongata. However, no such decline could be observed after 2 consecutive daily injections of morphine. In the cerebral cortex there was a significant decline (p less than 0.01) in ChAT activity after the second administration of morphine. These findings indicate that the changes in the responsiveness of the brain cholinergic enzymes following repeated morphine administration may in part explain the rapid development of tolerance to the analgesic effect of morphine.
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PMID:Brain cholinergic involvement during the rapid development of tolerance to morphine. 358 57

The action of electroacupuncture (EA) may be similar to analgesia by electrode stimulation or transcutaneous nerve stimulation. Since EA may directly stimulate nerve activity or indirectly enhance the release of opiate peptides and other neurotransmitter substances, we have used (Na+ + K+)-ATPase as a model to study the mechanism of action of EA. The membrane-bound (Na + K)-ATPase from purified synaptic plasma membranes inhibited slightly by high concentration of endorphin (30 microM), but not by met-enkephalin up to 6 X 10(-4) M. A single EA treatment for 30 min did not alter the (Na+ + K+)-ATPase activity in the cerebral cortex. However, when rats were treated with low (4 Hz) or high (200 Hz) frequency EA 30 min daily for 3 weeks, both (Na+ + K+)-ATPase and acetylcholinesterase were significantly elevated. The enhanced (Na+ + K+)-ATPase activity after high frequency EA was only partially blocked by i.p. injection of naloxone prior to EA during the last week of the EA treatment program. The results indicated that EA treatment may involve some other neurotransmitter pathways besides opiate peptides.
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PMID:Effect of electroacupuncture on synaptosomal (Na+ + K+)-ATPase. 614 70

Soman (50 micrograms/kg) and sarin (120 micrograms/kg), potent organophosphate anticholinesterase agents, produced an analgesic response in the mouse hotplate latency test. Naloxone antagonized but did not completely reverse the soman- and sarin-induced analgesia, whereas atropine antagonized completely the soman-and sarin-induced analgesia. Soman poisoning did not potentiate morphine-induced analgesia. It was simply an additive response. In survivors of soman (287 micrograms/kg) poisoning, the analgesia was more pronounced and was still apparent 96 hr after administration. This analgesia was completely antagonized by naloxone. Similar results were found in survivors of sarin (510 micrograms/kg) poisoning. The organophosphate-induced analgesia was not due to physical incapacitation as evidenced by performance on the accelerating rotorod. It is suggested that the organophosphate-induced analgesia is due to a combination of an increased concentration of acetylcholine due to inhibition of acetylcholinesterase combined with a reduced destruction of endogenous opioid-like substances due to organophosphate inhibition of proteases.
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PMID:Soman and sarin induce a long-lasting naloxone-reversible analgesia in mice. 670 39

2,5-Hexanedione is a n-hexane metabolite with neurotoxic properties. We have previously demonstrated that acute administration of 2,5-hexanedione causes analgesia in the tail-flick test in rats. In the present investigation, we examined the possible involvement of a cholinergic component in the 2,5-hexanedione-induced antinociception, since literature data indicate that this hexacarbon compound may act as a competitive inhibitor of acetylcholinesterase and that cholinesterase inhibitors are analgesic to rodents. Rats were treated with saline or with 5 or 25 mg/kg atropine (intraperitoneally) 10 min. before the injection of vehicle or 800 mg/kg 2,5-hexanedione (intraperitoneally). 2,5-Hexanedione caused a significant increase in tail-flick latencies at 10, 30, 60 and 90 min. after hexacarbon injection. Atropine (5 or 25 mg/kg) partially reversed the analgesia caused by 2,5-hexanedione at 60 and 90 min. When effects of 2,5-hexanedione on brain acetylcholinesterase was assessed in vitro, the results demonstrated that a competitive component is involved in enzyme inhibition. Taken together, these data support the involvement of a cholinergic (muscarinic) component in 2,5-hexanedione-induced analgesia.
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PMID:Atropine reverses antinociception induced by 2,5-hexanedione in rats. 858 10

Intravenous metoclopramide potentiates the analgesic effects of opioids in postoperative patients. We speculate that increased spinal concentrations of acetylcholine from metoclopramide-induced acetylcholinesterase inhibition is the mechanism responsible for enhanced morphine analgesia from metoclopramide. Sixty patients undergoing elective cesarean section with subarachnoid anesthesia were randomized to receive either 20 mg metoclopramide or saline intravenously 30-60 min prior to subarachnoid injection. Prior to subarachnoid injection of local anesthetic, 2 mL of cerebrospinal fluid (CSF) was aspirated for cholinesterase activity measurement. Visual analog scale (VAS) scores for pain were obtained prior to drug administration, at first patient request for analgesia, and at discharge from the postanesthesia care unit. Total morphine use was recorded in the recovery room and for 24 h postoperatively. There were no significant differences in VAS scores, morphine use, or CSF cholinesterase activity between groups. CSF cholinesterase activity was similar to values in nonpregnant patients demonstrated previously. This study failed to confirm the morphine-enhancing action of 20 mg intravenous metoclopramide in postoperative patients. Furthermore, this dose of metoclopramide does not inhibit CSF acetylcholinesterase.
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PMID:Bolus metoclopramide does not enhance morphine analgesia after cesarean section. 861 Aug 62


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