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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneously elevated nociceptive threshold levels were markedly diminished after Naloxone injections in 4 patients with congenital insensitivity to pain. This finding suggested the hypothesis of a relation between congenital insensitivity to pain and permanent hyperfunction of an endomorphinic system. Radio-immunoassay of CSF beta-endorphin was performed in all 4 cases. The normal or only slightly elevated levels cannot explain electrophysiologic findings, but as a function of the multiplicity of endogenous opioid systems, hyperactivity of another endomorphinic system cannot be excluded. Other hypotheses may also be proposed.
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PMID:[Cerebrospinal fluid beta-endorphin in congenital insensitivity to pain]. 243 47

In a patient with advanced cancer, neurosurgery relieved severe pain that had been uncontrolled by very high doses of opioids. On reduction of opioid dosage he had visual and auditory hallucinations and showed deterioration of consciousness progressing to coma. Naloxone worsened his mental state whereas morphine restored it to normal. This syndrome may be related to opioid withdrawal at receptors other than the mu receptors that have been linked to analgesia and drug abuse.
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PMID:Unusual opioid withdrawal syndrome. A case-report. 243 13

Previous investigations find that morphine administered i.c.v. induces antinociception directly at supraspinal sites and indirectly via activation of descending spinal systems. Independent experimentation suggests substance P and N-methyl-D-aspartate (NMDA) administered intrathecally (i.t.) can act as putative pain neurotransmitters to stimulate afferent pathways mediating nociception. The present studies were designed to determine whether a functional link exists between these observations. Mice were administered morphine i.c.v. 15 min before i.t. injections of substance P or NMDA. Additional investigations utilized coadministration of substance P or NMDA i.t. with one of several antagonists. Morphine administered i.c.v. inhibited both substance P- and NMDA-induced behavior in a dose-dependent manner. Coadministration of noradrenergic or adenosine receptor antagonists with substance P or NMDA i.t. dose-dependently reversed morphine (i.c.v.)-mediated inhibition. Methysergide injected i.t. caused significant, but only partially effective, antagonism of the effects of morphine (i.c.v.). Naloxone coadministered i.t. was effective in reversing morphine (i.c.v.)-mediated inhibition of NMDA-induced behavior, but ineffective in the substance P assay. These data demonstrate a functional link between activation of descending systems mediating antinociception by morphine (i.c.v.) and inhibition of putative pain neurotransmitters by spinally active antinociceptive agents. The potential involvement of serotonergic and opioid spinal systems is not clear, but noradrenergic and adenosine spinal pathways appear to play an important role in the indirect actions of morphine (i.c.v.). Differences in the inhibition of NMDA- and substance P-induced behavior also provide evidence for the presence of substance P and NMDA receptors in separate afferent pathways transmitting nociceptive stimuli.
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PMID:Morphine (intracerebroventricular) activates spinal systems to inhibit behavior induced by putative pain neurotransmitters. 248 Oct 30

Numerous reports indicated that substance p (SP) was a neurotransmitter involved in nociception, it also had analgesic effects in the most part of the central nervous system of all mammals, including man. The numbers of mast cell in human's some acupoint tissue were much higher than the non-acupoint tissue, there was connection between the nerves and mast cells which contained SP particles. Therefore, it is worth studying the change of the concentration of SP in the skin and plasma of rats during the process of acupuncture analgesia. 55 rats were divided into 8 groups; (1) Control group; (2) Heat stimulation group; (3) Electro-acupuncture group; (4) Morphine group; (5) Naloxone (NX) group; (6) NX plus electro-acupuncture group; (7) Non-acupoint electro-acupuncture group; (8) Normal saline solution group. The concentration of SP in the "channel" "acupoint" skin and plasma of rats were determined by radioimmunoassay (RIA). The results show that after acupuncture, the tail-flick threshold is increased, the concentration of SP in the skin and plasma is decreased significantly and the effect of electro-acupuncture is abolished by naloxone (i.p). The results suggest that SP is a transmitter relating to skin nociception and involves the process of pain regulation. Electro-acupuncture can inhibit SP release from the skin and the plasma of rats. There is a functional interaction between SP and endorphin in the effects of electro-acupuncture. That is the SP decreased induced by electro-acupuncture may depend upon the function of opiate receptors.
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PMID:[The change of the concentration of substance P in the rats "channel" "point" skin and plasma in the acupuncture analgesia]. 248 85

Sixty-six patients undergoing total knee arthroplasty were offered epidural morphine as a method of postoperative analgesia. Of the 66 patients, 50 completed the minimum protocol of 3 days in a special epidural monitoring unit and were thus available for study. In this study group, 86% stated that they obtained 75-100% relief of pain with each epidural injection. Greater than 90% of the patients rated the overall experience with epidural analgesia as excellent or good. Ninety percent stated that they would choose epidural morphine analgesia again if given the choice. Nausea and vomiting were the most common adverse effects, occurring in 34%. One patient experienced respiratory depression, which was reversed with Narcan. The most frequent complaint related to the procedure itself was the use of an apnea monitor; 18% of the patients considered this monitoring device intolerable. The progress of total knee arthroplasties in the epidural unit was monitored by range of motion achieved. At 72 hours the average motion was 10 degrees-87 degrees and at the end of the hospital stay was 6 degrees-98 degrees. The total hospital bill for epidural morphine analgesic patients was $469 more than for a conventional arthroplasty patient, though the mean duration of hospital stay was 1.7 days less for the epidural morphine patients. Epidural morphine provided excellent but inconsistent postoperative pain relief. When relief was present, aggressive in-house rehabilitation could be instituted, and a shorter overall hospital stay was achieved when compared with conventional analgesia. Nonetheless, the related adverse effects and inconsistent pain relief on many patients may preclude the use of epidural morphine as a single postoperative analgesic agent.
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PMID:The use of epidural morphine in patients undergoing total knee arthroplasty. 250 54

We studied the effect of nalbuphine on the ventilatory and occlusion pressure responses to carbon dioxide rebreathing in six healthy male volunteers (mean age 25.5 yr) in a single-blind laboratory study. On four separate days volunteers were assigned randomly to receive either placebo (0.9% sodium chloride) or three i.v. doses of nalbuphine (15, 30 and 60 mg 70 kg-1), followed 90 min later by naloxone 0.4 mg 70 kg-1. Duplicate rebreathing tests were performed and the mean intercept at PE'CO2 7 kPa and the slopes of the linear relationship between inspiratory minute ventilation (Vl) or occlusion pressure (P0.1) with PE'CO2 were measured. Nalbuphine significantly decreased the mean intercept of the Vl (P less than 0.01) and P0.1 (P less than 0.05) responses, but caused no changes in the slopes. No significant difference between the doses was noted, suggesting that an Effect maximum (E'max) for respiratory depression was reached with a dose of approximately 15 mg 70 kg-1. Naloxone was less effective in antagonizing the depression in Vl at the higher dose of nalbuphine. Similar P0.1 values were associated with the same inspiratory flow rate (1 litre s-1) before and after drug treatment, suggesting that nalbuphine acts centrally to depress ventilation. Sedation increased significantly following each dose of nalbuphine (P less than 0.001). No demonstrable difference between the doses was shown, suggesting an Effect maximum (E'max) for sedation was reached at about 15 mg 70 kg-1. Administration of nalbuphine was associated with pain at the injection site, dizziness, dreaming, nausea and vomiting. Cardiovascular stability was maintained in all subjects.
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PMID:Effect of nalbuphine hydrochloride on the ventilatory and occlusion pressure responses to carbon dioxide in volunteers. 250 65

Rats were randomly divided into 4 groups: Control, Electro-acupuncture (EA), Naloxone and Naloxone plus EA. The content of noradrenaline (NA) and dopamine (DA) in brain stem, diencephalon and telencephalon were determined by spectrofluorometry. It was found that the pain threshold increased and the NA content in the telencephalon decreased and the DA level in the brain stem increased markedly after EA. Naloxone injection partially decreased the analgesic effect of EA and abolished the EA-induced elevation of DA in the brain stem and attenuated the NA level in the diencephalon after EA. These results suggest that morphine receptor may play an important role in EA analgesia and this may be partially carried out through the brain catecholamine system.
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PMID:[Effects of intraperitoneal injection of naloxone on the analgesic effect and the changes of brain catecholamine contents induced by electroacupuncture in rats]. 251 24

In this paper the averaged cortical evoked potential (C-CEP) induced by stimulating the C-fibers of the splanchnic nerve was used as an index of visceral pain to further study the effects of acupuncture and morphine on it. Experiments were carried out on 35 cats anesthetized with chloralose and immobilized with flaxedil. The splanchnic nerve was stimulated with electric pulses of varied strength and blocked by a galvanic current so as to cause A- or C-fibers input selectively. The cortical evoked potential was recorded on the contralateral post-sigmoid gyrus and averaged by TQ-19 Medical Data Processor. The compound action potential of splanchnic nerve was monitored. "Neiguan" acupoint was stimulated with electric pulses (0.1ms, 4v and 5Hz). The results were as follows: 1) when "Neiguan" acupoint, was excited with the electric pulses, C-CEP and the late component of A-CEP which was evoked by stimulating A-fibers of splanchnic nerve were obviously reduced in amplitudes. It was suggested that electro-acupuncture (EA) of "Neiguan" acupoint could inhibit visceral pain (the slow and fast pain). 2. After intravenous injection of morphine, the amplitudes of C-CEP and the late component of A-CEP were depressed significantly, indicating that C-CEP might reflect the visceral slow pain and the late component of A-CEP reflect the fast pain. 3. Naloxone could block partially the inhibitory effect of EA of "Neiguan" acupoint on C-CEP, suggesting that the inhibition of EA might be associated with the release of endogenous opiate like substances.
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PMID:[The effect of electro-acupuncture of "neiguan" acupoint on cortical potential evoked by stimulating C-fibers of splanchnic nerve]. 251 2

Effects of yohimbine, methysergide and naloxone given intrathecally (i.t.) and naloxone given intracerebroventricularly (i.c.v.) on inhibition of the tail-flick and hot-plate response induced by beta-endorphin and morphine given i.c.v. were studied in male ICR mice. Yohimbine (1.5 and 15 micrograms) and methysergide (1.5 and 15 micrograms) injected i.t. antagonized inhibition of the tail-flick response induced by morphine but not beta-endorphin administered i.c.v. On the other hand, naloxone (20 ng) injected i.t. antagonized inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin but not morphine. Yohimbine and methysergide given i.t. did not antagonize inhibition of the hot-plate response induced by morphine nor did naloxone given i.t. antagonized i.c.v. beta-endorphin-induced inhibition of the hot-plate response. Naloxone given i.c.v. was more effective in antagonizing morphine-induced inhibition of the tail-flick and hot-plate response than inhibition induced by beta-endorphin given i.c.v. Naloxone at doses (0.1 and 1 microgram) which effectively reversed inhibition of the tail-flick response to i.c.v. morphine was not effective in reversing the i.c.v. beta-endorphin-induced inhibition of the tail-flick response. Our results indicate that beta-endorphin and morphine produce analgesia by stimulating separate types of opioid receptors, epsilon- for for beta-endorphin and mu- for morphine, and activate separate descending pain modulatory control systems. The supraspinal epsilon system stimulated by beta-endorphin is mediated by activation of spinal opioid receptors whereas the supraspinal mu system stimulated by morphine is mediated by activation of spinal alpha 2-adrenoceptors and serotonin receptors for the production of analgesia.
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PMID:Differential mechanisms mediating beta-endorphin- and morphine-induced analgesia in mice. 253 Oct 93

In a recent study [30] it was reported that naloxone, at doses normally employed for opioid antagonism, produced a dose-dependent analgesia in BALB/c mice in the formalin test. We report here that another opioid antagonists, naltrexone, also produces analgesia under these conditions. Female BALB/c mice were injected subcutaneously with naltrexone (0.01-1.0 mg/kg) or saline alone and tested for analgesia using the formalin test. Naltrexone produced a statistically significant dose-dependent analgesia, with an ED50 of 0.05 mg/kg and almost total analgesia at doses of 0.1 mg/kg or greater. To determine the relationship between naloxone analgesia and better documented forms of opioid analgesia, BALB/c mice were injected with naloxone or saline following the administration of a pre-determined ED50 for morphine and tested for analgesia using the tail-flick and formalin tests. Naloxone antagonized morphine analgesia in the tail-flick test at both doses used (0.3 and 10 mg/kg). In the formalin test, however, naloxone attenuated morphine analgesia at the lower doses (0.1 and 0.3 mg/kg) and potentiated morphine analgesia at the highest dose (10 mg/kg). The implications of this finding are discussed.
Pain 1989 Jan
PMID:Analgesia produced by normal doses of opioid antagonists alone and in combination with morphine. 253 85


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