Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of intractable pain with parenteral, subarachnoid, or epidural narcotics is often unsatisfactory due to tolerance and other systemic complications that accompany increasing dosages of these drugs. Other disadvantages include the potential infections with implantable pumps and the inconvenience of repeated narcotic administration. During the past several years, studies at the author's laboratory indicated that transplantation of adrenal medullary tissue or isolated chromaffin cells into the spinal subarachnoid space can significantly reduce pain in several rodent models without resulting in development of tolerance. Adrenal medullary chromaffin cells were selected because they produce high levels of both opioid peptides and catecholamines, agents that independently, and possibly synergistically, reduce pain when injected locally into the spinal subarachnoid space. The adrenal medullary transplants survive for prolonged periods, and continue to produce high levels of both catecholamines and met-enkephalin. These transplants reduce pain in two rodent chronic pain models, an arthritis model and a peripheral neuropathy model, both of which closely resemble human chronic pain syndromes. The success of the animal studies has led to initiation of human clinical trials in patients with chronic cancer pain; results are promising.
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PMID:Chromaffin cell transplants for alleviation of chronic pain. 137 36

We have investigated plasma beta-endorphin (beta-E), ACTH, and cortisol in two cases of congenital indifference to pain (CIP), a rare syndrome characterized by unresponsiveness to painful stimuli. As the two patients had frequent skin infections, we also studied lymphocyte response to mitogens in the absence or presence of beta-E. In addition, we explored a series of lymphocyte membrane antigens related to different aspects of the immune response, such as CD3+, CD4+, CD8+, B, NK Leu 7, Leu 9, and Leu 19, anti-interleukin-2 receptor (anti-TAC). Plasma beta-E levels in the two patients were significantly higher than in controls, whereas plasma ACTH and cortisol levels were normal. Lymphocyte response to the mitogen phytohemagglutinin was normal. The expression of Leu 7, Leu 9, and Leu 19, three antigens related to natural killer cells, was decreased by about 50%. The results indicate that in the two cases of CIP studied, high plasma beta-E levels are associated with a reduction in the expression of natural killer cells. This suggests that the two phenomena are specifically related to each other. These data represent further evidence of the possible pathophysiological relevance of the neuroendocrine-immune feedback.
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PMID:Plasma beta-endorphin levels and natural-killer cells in two cases of congenital indifference to pain. 137 38

Effects of dorsal root entry zone lesions (DREZLs) on cerebrospinal fluid (CSF) and plasma concentrations of neuropeptides, catecholamines, and cyclic nucleotides were studied in 9 patients with intractable chronic pain. Contents of beta-endorphin-like-material in CSF decreased in all patients 12-17 days following DREZLs during which complete to good pain relief was achieved. Contents of beta-endorphin-like-material in CSF increased again about one month after DREZLs in two and remained unchanged in one of three patients tested, who complained of partial reappearance of pain. Contents of beta-endorphin-like-materials in plasma showed no significant changes after DREZLs. Substance P, noradrenaline, adrenaline, and cyclic nucleotide levels in both CSF and plasma were variable among the subjects and did not change significantly following the operations. Thus, the results suggest that production of beta-endorphin-like-material in the central nervous system is decreased by DREZL, though the increase in its turn-over might not be neglected. The mechanisms of the decrease in contents of beta-endorphin-like-material in CSF after DREZLs were discussed in terms of our current knowledge of pain and pain inhibitory systems.
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PMID:Effects of dorsal root entry zone lesions on CSF and plasma neuropeptides and catecholamines. 138 Nov 37

To determine the possible role of endogenous opioid peptides in the action of imipramine and paroxetine in painful diabetic neuropathy, beta-endorphin concentrations in plasma were measured in 20 patients during a double-blind, placebo-controlled randomized three-way crossover trial. Despite a significant reduction in neuropathy symptoms during both imipramine and paroxetine treatment, the beta-endorphin level was unaltered throughout the study. The plasma concentration of beta-endorphin was not related to plasma drug concentrations. Thus, this study does not provide evidence of a role of endogenous opioid peptides in the mechanism of action of imipramine and paroxetine in painful diabetic neuropathy.
Clin J Pain 1992 Jun
PMID:Plasma beta-endorphin is not affected by treatment with imipramine or paroxetine in patients with diabetic neuropathy symptoms. 138 95

Cluster headache is a disorder of unknown origin. Some studies have focused their attention on neuroendocrine derangement, others on immunity. To probe central alterations in cluster headache (CH), immune parameters were investigated in cluster headache patients in comparison to low back pain patients and healthy controls. Increases in peripheral blood monocytes found in remission cluster headache patients may be attributable to chronic central nervous system (hypothalamic?) noradrenergic dysfunction or altered beta-endorphin. Alterations in NK+, CD3+ and CD4+ levels found in cluster period cluster headache and low back pain patients are probably pain or stress-related.
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PMID:Immunological alterations in cluster headache during remission and cluster period. Comparison with low back pain patients. 138 94

The results from recent studies suggest that the endogenous opioid beta-endorphin (beta-E) is related to pain modulation. Therefore, plasma beta-E levels were studied in 23 patients with essential hypertension (EH) and in 7 patients with coronary artery disease (CAD) during asymptomatic ischemic events and in 5 patients with CAD during symptomatic ischemic events. Blood samples for beta-E were taken at the moment of silent ST depression, pointed with alarm by the real time ECG monitor "Q Med Monitor" (USA). Control blood samples were taken under the same conditions without ischemic events. Control plasma beta-E levels were significantly higher (p less than 0.01) in patients with EH as compared to that in both groups of patients with CAD (22.9 +/- 4.0 vs 7.0 +/- 1.9 and 4.5 +/- 1.6 pmol/l). At the time of silent ischemia, beta-E showed a significant increase in patients with EH (+10.1 +/- 2.1 pmol/l, p less than 0.01) and in patients with CAD (+10.7 +/- 1.3 pmol/l, p less than 0.05) as compared to the control levels. However, plasma beta-E showed no increase (+1.0 +/- 0.6 pmol/l, p greater than 0.1) during symptomatic ischemia as compared to the control levels. Thus, differences in the circulating levels of beta-E may be associated with the presence or absence of pain during myocardial ischemia.
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PMID:[Plasma beta-endorphin level in "silent" myocardial ischemia during Holter ECG monitoring]. 140 1

Previous studies from this laboratory suggested that the periaqueductal gray (PAG), nucleus accumbens, and amygdala might take part in a serial, unidirectional mesolimbic loop to play their roles in pain modulation. It has been proposed that morphine injected into one of these nuclei would cause the release of opioid peptides in one nucleus after another. This working hypothesis was examined in the present study by perfusing simultaneously the PAG and the amygdala after microinjection of morphine into the N. accumbens. It was found that microinjection of morphine increased the content of immunoreactive enkephalins (ir-ENK) and immunoreactive beta-endorphin (ir-beta-EP) in the perfusate of the PAG and the amygdala. When the perfusion fluid contained 3 microM of naloxone, the increase of ir-ENK and ir-beta-EP was reduced significantly. These results indicate that the three nuclei were not serially connected in a unidirectional loop.
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PMID:Naloxone blocks opioid peptide release in periaqueductal gray and amygdala elicited by morphine injected into N. accumbens. 140 5

Thirty cancer patients, clinical group IV, have been examined. It has been established that a persistent pain syndrome leads to lowering in beta-endorphin liquor level. Morphine analgesia is followed by beta-endorphin level elevation which directly depends on pain intensity and analgesia efficacy. Determination of changes in beta-endorphin liquor level may serve as a criterion of analgesia efficacy.
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PMID:[Changes in the concentration of beta-endorphin in the cerebrospinal fluid due to morphine analgesia in incurable oncologic patients]. 141 98

Blood plasma levels of "pain substances" (serotonin, histamine, prostaglandin F2 alpha, adrenaline /A/) and neuropeptides (beta-endorphin, somatostatin) have been evaluated in 39 patients during the early postoperative period after lung and mediastinum surgery. The studies have shown that the content of these biologically active substances increases considerably. Following stellate ganglion blockade A concentration decreased significantly, the uptake of narcotic analgesics used for postoperative analgesia reduced 1.7-fold, however the levels of "pain substances" and neuropeptides remained unchanged. It is believed that postoperative pain syndrome develops due to the elevation of the levels of the substances under study. Stellate ganglion blockade produces only sympatholytic effect, which shows the necessity of the elaboration of drug therapeutic techniques blocking "pain" receptors and using "pain substance" antagonists.
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PMID:[The role of humoral factors in the pathogenesis of the postoperative syndrome]. 146 32

Piroxicam is a nonsteroidal anti-inflammatory drug with a potent analgesic effect. In order to establish whether the analgesic action of Piroxicam has a central component, we studied the effect of the drug on the nociceptive orbicularis oculi reflexes evoked by electrical stimulation of the cornea and supraorbital nerve in healthy subjects. Piroxicam significantly suppressed the corneal reflex and R3 component of the blink reflex by 28% (p < 0.05) and 50% (p < 0.01), respectively. This effect was not reversed by the i.v. injection of naloxone. Beta-endorphin levels did not change. Piroxicam administration induces distinct inhibitory changes in nociceptive reflexes, which suggests that the analgesic action of the drug has a central component. The ineffectiveness of naloxone, and the lack of beta-endorphin changes, indicate that this central action is independent of the opioid system; other pain regulatory systems are probably involved.
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PMID:Piroxicam-induced analgesia: evidence for a central component which is not opioid mediated. 147 79


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