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

The article systematically reported our physiological and biochemical work on the relationship between central acetylcholine and acupuncture analgesia. The results indicate: 1. Acupuncture on acupoints could produce analgesia. 2. Ach contents in cerebrospinal fluids and brain increased under acupuncture analgesia. 3. AChE activities iu brain elevated under acupuncture analgesia. 4. ChE inhibitor reinforced the effects of acupuncture and inhibitor of ACh synthesis could inhibit the effects of acupuncture, which could be reversed by administration of ACh and chlorocholine. M-AChR antagonists could also inhibit the effects of acupuncture. 5. The turnover rate of ACh in diencephalon, caudate nucleus and spinal dorsal horn accelerated when acupuncture analgesia. The discussion was given on the variation of metabolic dynamics in combination with related literature.
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PMID:[Research on the relationship between central acetylcholine and acupuncture analgesia]. 191 33

The spinal ganglion a cell body storage of somatic primary-sensory neurons, is considered as an important region for neurochemical research of primary afferent nerves. The present experiment aims at the observation on the Ach content and its changes in the ganglia of 128 rats by means of biochemical methods under the effect of administration of Neostigmini and application of electroacupuncture. It is found that there are evidence of existence of Ach in the ganglia and when the AchE activity in the periphery nerve system is inhibited, the Ach content of ganglia rose. In addition, during acupuncture (applied at acupoint "Huantiao") analgesia, no apparent changes of Ach content can be visualized in spinal ganglia, however, the level of AchE activity goes up evidently. The foregoing results indicate that in the somatic primary-sensory neuron Ach is one of important neurotransmitters which may influence and take part in the transmission of sensory information through primary afferent nerves.
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PMID:[Influence of electroacupuncture on ACh content and AChE activity in the spinal ganglia of rat]. 251 10

1. In cats under light allobarbitone anaesthesia, the effects of intravenous injections of narcotic and non-narcotic analgesics, of a general depressant, and of narcotic antagonists were investigated on the spontaneous release of acetylcholine (ACh) from the surface of the sensorimotor cortex.2. The narcotic analgesics morphine (0.1, 1.0 and 5 mg/kg), meperidine (1.0 and 2.0 mg/kg), methadone (1.0 mg/kg) and codeine (5.0 and 10.0 mg/kg) greatly reduced ACh release.3. The non-narcotic analgesics pentazocine (1.0 and 2.0 mg/kg) and propoxyphene (5.0 and 10.0 mg/kg) as well as the depressant chlorpromazine (0.25, 0.5 and 1.0 mg/kg) also greatly reduced ACh release.4. Two of the three narcotic antagonists examined, levallorphan (0.1, 1.0 and 5 mg/kg) and nalorphine (1.0 mg/kg) had the property of reducing ACh release. They were thus partial agonists. With levallorphan the greatest reduction occurred with the smallest dose injected and the effect was regularly obtained, whereas with nalorphine a reduction was obtained in some experiments only. The third, naloxone, was a specific narcotic antagonist and did not reduce the ACh release in any dose (0.01, 0.1, 0.5 and 1.0 mg/kg) examined. In a dose of 1.0 mg/kg it actually produced a small increase in Ach release.5. Naloxone (0.1-1.0 mg/kg) restored the reduction in ACh release produced by the narcotic analgesics and by the partial agonist levallorphan. It partially restored the reduction produced by the non-narcotic analgesics and by nalorphine, but had no effect on the reduction produced by chlorpromazine.6. The relevance of these results with regard to analgesia and to the narcotic abstinence syndrome is discussed.
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PMID:Effects of narcotic analgesics and antagonists on the in vivo release of acetylcholine from the cerebral cortex of the cat. 513 64

Clonidine, when administered for prolonged period showed no tolerance to its analgesic activity. Prior exposure to clonidine attenuated the tolerance development to morphine-induced analgesia and the supersensitivity to acetylcholine (ACh) in ileum during chronic morphine treatment. Further, acute administration of lower doses of clonidine (upto 1 mg) produced supersensitivity in ileum to Ach while the higher dose (10 mg) induced subsensitivity. In vas deferens, clonidine in all the concentrations tested induced dose and time dependent supersensitivity to norepinephrine (NE) similar to that produced by morphine. Chronic clonidine treatment failed to alter the ACh responses in ileum while it produced supersensitivity to NE in vas deferens. The results suggest that clonidine and morphine possess comparable properties and the antagonism of chronic morphine tolerance by clonidine may be the therapeutic basis for its clinical application in the treatment of opiate addicts.
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PMID:Effect of clonidine on the chronic morphine tolerance and on the sensitivity of the smooth muscles in mice. 688 70

This article reviews the main results in recent years of studies on the role of central Ach in pain modulation and analgesia, including: (1) cholinergically induced analgesia (CIA). Cholinomimetic drugs raised the pain threshold or inhibited the unit discharges of hypothalamus parafascicularis nuclens in rats, and these actions were revised by atropine not by nicotine. (2) Ach and acupuncture analgesia (AA). The effect of electroacupuncture was changed by administration of HC-3, atropine, etc. (3) Ach and stress analgesia (SA). Scopolamine reduced the hind foot shock induced analgesia, and this kind of SA was probably mediated by m-receptors existed at supraspinal, rather than spinal level. Swimming and immobilization analgesia were also related to Ach. These data suggested that the central cholinergic system is very important in pain modulation and analgesia and the central Ach is essential transmitter or modulator in this analgesic pathway. But the problem is whether the mechanism of CIA is involved in opiate analgesic system or not.
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PMID:[The role of Ach in the central nerve system on pain modulation and analgesia]. 808 73