Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta-Endorphin administered intrathecally (i.t.) in rats produced a dose-dependent elevation in tail-flick latency. Naltrexone administered i.t. as a pretreatment reversed the spinal antinociceptive action of beta-endorphin, suggesting that the opioid interacts directly with spinal opiate receptors. Spinal administration of the alpha 1-adrenoceptor antagonist WB-4101 failed to alter the analgesic effects of the opioid, whereas the alpha 2-adrenoceptor antagonist yohimbine completely blocked beta-endorphin-induced elevations in tail-flick latency. Thus, there is an apparent specificity for the alpha 2-adrenoceptor to mediate the spinal action of beta-endorphin. The 5-HT1 and 5-HT3 receptor antagonists (spiroxatrine and ICS 205-930, respectively) also reversed the analgesic effects of the opioid, while the 5-HT2 receptor antagonist ritanserin only partially blocked beta-endorphin-induced elevations in tail-flick latency. The present results suggest that beta-endorphin produces analgesia at the spinal level via an opiate receptor-mediated interaction with spinal monoaminergic nerve terminals.
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PMID:Spinal beta-endorphin analgesia involves an interaction with local monoaminergic systems. 256 5

gamma-Endorphin-type peptides (i.e. gamma-endorphin, des-tyr'-gamma-endorphin [DT gamma E]) result from the processing of the opioid peptide, beta-endorphin. Previous studies have implicated the involvement of beta-endorphin in various types of shock, including anaphylactic shock. In the present experiments the intracerebroventricular (i.c.v.) administration of gamma-endorphin (10 micrograms) or DT gamma E (3.3-10 micrograms) significantly improved survival in anaphylactic shock in mice. Moreover, DT gamma E (10 micrograms) reversed the effect of i.c.v. beta-endorphin (3.3 micrograms) to exacerbate shock. A similar dose of DT gamma E was ineffective in antagonizing beta-endorphin-induced analgesia. The anti-anaphylactic action of DT gamma E as well as its effect to block the pro-anaphylactic action of beta-endorphin were prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride. The results suggest that gamma-endorphin-type peptides may act in the central nervous system (CNS) to physiologically oppose the autonomic pathophysiologic influences of beta-endorphin.
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PMID:Beneficial effect of gamma-endorphin-type peptides in anaphylactic shock. 257 12

The present study was performed to explore the possible involvement of the arcuate nucleus of hypothalamus (ARH) and beta-endorphinergic pathway in the connection from nucleus accumbens to periaqueductal grey (PAG). It was found that the analgesic effect of morphine administered to nucleus accumbens of the rabbit was significantly attenuated by the antiserum against beta-endorphin (beta-EP) injected into PAG. The antagonistic effect was totally abolished by lesioning of the ARH. However, in the rabbit with ARH lesioning, no significant change in basal nociceptive threshold was seen nor was there any significant change in the efficacy of analgesia induced by injecting morphine into nucleus accumbens. The latter effect was attenuated by intra-PAG-administered naloxone, as in the normal control rabbits. These results indicate that (1) ARH and its efferent beta-endorphinergic fibers are involved in the descending pathway from the nucleus accumbens to PAG, subserving an antinociceptive effect, (2) endogenous opioid peptides other than beta-EP seem to play an equally important role in mediating analgesia.
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PMID:Involvement of arcuate nucleus of hypothalamus in the descending pathway from nucleus accumbens to periaqueductal grey subserving an antinociceptive effect. 258 31

The concentrations of endogenous opiates (beta-endorphin, methionine-enkephalin, leucine-enkephalin) in the spinal fluid and arterial blood plasma has been studied in 16 dogs, using the model of acute pain stimulation under electroacupuncture analgesia (EAA). It has been shown that pain stimulation under EAA is accompanied by a significant increase in methionine-enkephalin++ and leucine-enkephalin concentrations (by 244 and 69.4%, respectively) in the spinal fluid. beta-endorphin level tends to increase. There is also a trend towards the reduction in beta-endorphin and methionine-enkephalin concentrations in the arterial blood plasma, which is indicative of effective antinociceptive stimulation of the endogenous opiate system. However, by the end of the first hour a decrease of methionine-enkephalin and leucine-enkephalin levels in the spinal fluid was paralleled by a trend towards beta-endorphin and methionine-enkephalin increase and a significant leucine-enkephalin increase in arterial blood plasma, which can account for the exhaustion of the opiate system.
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PMID:[Changes in the concentration of endogenous opiates in the blood and cerebrospinal fluid during acute painful stimuli and protective electroacupuncture analgesia]. 262 35

Opioid activity of a homologous series of met-enkephalin alkylamides was analysed. In guinea pig ileum test, the hexylamide derivative was most active, whereas the isopropylamide derivative was most potent in analgesia test. The results suggest that structural changes of this type at the C-terminus of the pentapeptide improve the opioid activity.
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PMID:Morphine-like activity of some N-substituted amides of met-enkephalin. 263 4

Plasma levels of cortisol, ACTH and beta-endorphin like immunoreactivity (beta-ELI) were measured to evaluate postoperative pain relief with epidural morphine and systemic analgesics in conjunction with endocrine functions in 16 patients who underwent gastrectomy. Eight of these patients (epidural morphine group) obtained postoperative analgesia with continuous epidural infusion of morphine with a pump as in our previous report. A bolus of epidural morphine was administered through an indwelling thoracic (Th8,9) catheter at 3 hrs prior to the proposed end of the surgery, which was followed with continuous epidural infusion of morphine at a rate of 0.167-0.042 mg.hr-1 with a pump (CADD-PCA, Model 5200P, Pharmacia) during and after anesthesia and surgery with gradual decrease in dose until the third postoperative day. The remaining eight patients (systemic analgesics group) repeatedly received systemic pentazocine and buprenorphine when needed. Plasma cortisol levels increased significantly at the end of surgery and after in both groups. However plasma concentrations of cortisol in the epidural morphine group were significantly lower than those in the systemic analgesics group on the first and second postoperative days. Plasma levels of ACTH and beta-ELI increased significantly at the end of surgery but returned to levels of the previous day in both groups postoperatively. Our study suggests that continuous epidural infusion of morphine is adequate for postoperative pain relief and has suppressing effect on plasma cortisol levels as compared with systemic analgesics regimen.
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PMID:[Effect of continuous epidural infusion of morphine for postoperative analgesia on pituitary-adrenocortical function]. 277 49

The hypothesis that nitrous oxide stimulates the central pro-opiomelanocortin system in vivo was explored in this study. A concentration-dependent stimulation of central pro-opiomelanocortin neuropeptides was demonstrated after exposures to variable concentrations of nitrous oxide with oxygen. Rats exposed to 60% and 80% nitrous oxide with oxygen demonstrated an elevation of beta-endorphin concentration along the neuraxis involved with analgesia; no similar effect was observed in alpha-MSH concentration, neither duration of exposure nor acclimation to the enclosed environment altered this stimulation. The discontinuation of nitrous oxide exposure resulted in the diminution of beta-endorphin concentration to pre-exposure levels in 15-30 min. With an ACTH1-39 antisera, a semiquantitative increase in opiocortin immunoreactivity after exposures to nitrous oxide was demonstrated. In conclusion, the increase in beta-endorphin concentration and immunoreactive ACTH1-39 staining in the cells of origin, areas of fiber projection and terminal fields suggest that nitrous oxide stimulates the central pro-opiomelanocortin system in vivo in the rat.
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PMID:The effects of nitrous oxide on the central endogenous pro-opiomelanocortin system in the rat. 282 75

Stress in humans commonly results in gastrointestinal dysfunction, which is characterized by its symptomatology because the etiology is completely unknown. We developed an animal model in which to study the effects of stress on the gastrointestinal tract, and characterized the model as a stressor by evaluating endocrine and analgesic responses to mild restraint. Mild restraint (wrap restraint) elevated plasma levels of adrenocorticotropic hormone and beta-endorphin, and caused analgesia. The different regions of the gastrointestinal tract responded differently to the stress stimulus. Gastric emptying was not affected, small intestinal transit was inhibited, and large intestinal transit was stimulated by stress, and there was an associated increase in fecal excretion. Wrap-restraint stress did not result in the formation of ulcers. There was a strong correlation between stress-induced adrenocorticotropic hormone release and stress-induced intestinal dysfunction over a 24-h period that suggested a circadian influence. However, neither exogenous adrenocorticotropic hormone nor beta-endorphin had any effect on intestinal transit. Furthermore, neither adrenalectomy nor hypophysectomy prevented the response of the intestine to stress, suggesting that neither adrenal nor pituitary-derived factors are responsible for mediating the effects of stress on the gut. We conclude that wrap-restraint stress produces different effects on different regions of the intestine, suggesting that the small and large intestines are independently regulated and can respond differently to different stimuli. There were similarities between the intestinal effects of wrap-restraint stress in rats and intestinal symptoms associated with stress and irritable bowel syndrome in humans. Therefore, wrap restraint may be an appropriate animal model in which to study stress-related intestinal dysfunction. The mechanisms by which stress affects intestinal transit are still unresolved; however, the intestinal effects of stress are not mediated by either pituitary or adrenally derived factors.
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PMID:Stress-induced changes in intestinal transit in the rat: a model for irritable bowel syndrome. 282 44

The distribution of pro-opiomelanocortin (beta-endorphin, adrenocorticotropic hormone, and 16-K) neurons and fiber projections was evaluated immunocytochemically in 50-mu thick cryostat sections of human diencephalon and midbrain. Specific attention was focused upon regions in which deep brain stimulation has been most effective in the relief of selected chronic pain syndromes. This study revealed a remarkable, nearly point-to-point correlation between clinically effective stimulation sites and the distribution of pro-opiomelanocortin fibers in the human brain. Of particular interest was the dense innervation of the periventricular stratum along the third ventricle, the parafascicular centromedian region of the thalamus, and the periaqueductal gray matter of the midbrain. This study provides anatomical support for the hypothesis that beta-endorphin-containing neuronal systems may contribute to stimulation analgesia in the human.
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PMID:Immunocytochemical localization of pro-opiomelanocortin neurons in human brain areas subserving stimulation analgesia. 283 54

Stress can induce a naloxone reversible and a naloxone non reversible analgesia according to its parameters. We showed that naloxone non reversible analgesia can be reversed by antagonists of the kappa opiate receptor and that naloxone reversible analgesia can be related to mu receptors and beta-endorphin, while the kappa receptor mediated analgesia can be related to dynorphin. We have also shown that the characteristics of the receptors might change in consequence to stress and that the analgesic responses might be modulated by benzodiazepine agonists and antagonists.
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PMID:Endogenous opioids and their receptors in stress-induced analgesia. 285 67


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