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)

The contribution of central serotonergic pathways to the analgesic activity induced by salmon calcitonin in the writhing test was investigated. Salmon calcitonin was administered to mice after lesioning of the ascending and descending serotonergic pathways by means of i.p. administration of p-chloroamphetamine (40 mg/kg, for 2 days) or p-chlorophenylalanine (300 mg/kg, for 3 days). The analgesic effect induced by salmon calcitonin at the doses of 10 and 20 IU/kg was not evident in mice previously treated with p-chloroamphetamine or p-chlorophenylalanine. However, the analgesic effect of salmon calcitonin 40 IU/kg was not significantly modified by p-chloroamphetamine or p-chlorophenylalanine pretreatment. Salmon calcitonin did not alter the depletion of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid after p-chloroamphetamine or p-chlorophenylalanine administration. Similarly, this hormone did not change the NSD 1015-induced accumulation of 5-hydroxytryptophan or the tranylcypromine-induced accumulation of 5-HT. These results indicate that although salmon calcitonin does not influence the synthesis and metabolism of 5-HT, it does require the integrity of the serotonergic system in order to cause analgesia.
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PMID:Involvement of central serotonergic pathways in analgesia elicited by salmon calcitonin in the mouse. 751 26

1. When the analgesic effect of salmon-calcitonin (S-CT) and of eel-calcitonin (E-CT), as well as their influence on the morphine-analgesia were compared, no significant differences were found. 2. While on isolated tissues, E-CT induced a significant increase on the effect of bremazocine, [D-Pen2,D-Pen5]enkephalin and [Met5]enkephalin and no changes were observed on the effect of DAMGO, suggesting that E-CT increases the effects of opioids acting on delta or kappa receptors but not on mu receptors. 3. These findings corroborate the possibility of interactions between calcitonin and the opioid system.
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PMID:Analgesic effect of two calcitonins and in vitro interaction with opioids. 778 40

Calcitonin is a peptide hormone secreted by the C-cells of the thyroid gland. This hormone mainly acts in preventing bone resorption. Furthermore, calcitonin is involved in other biological actions, and in particular it is able to relieve pain independently of its peripheral effects on bone. Here, we examine the possible mechanisms of calcitonin-induced analgesia, with particular regard to the opioid system involvement. Several studies in animals and in humans demonstrate that calcitonin increases plasma beta-endorphin levels, acting at the hypothalamic and/or at the pituitary level, either directly or indirectly, through monoaminergic neurotransmitters. However, this calcitonin-induced beta-endorphin release has not always been observed. These different results are discussed, and a possible implication of sex and/or calcitonin dose employed has been examined. We conclude that the analgesic effects of calcitonin are multifactorial, and beta-endorphin plays its own specific role.
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PMID:Calcitonin and beta-endorphin secretion. 806 Dec 53

About 25% of U.S. women over age 50 will suffer one or more vertebral compression fractures related to osteoporosis. Vertebral fractures may be biconcave, anterior wedge, or crush deformities. A fracture is most often precipitated by putting a load on outstretched arms (eg, while raising a window). Back pain is usually incapacitating for a few weeks, then diminishes in severity but remains intense for 2 to 3 months. Acute complications include transient ileus, urinary retention, or (rarely) cord compression. Long-term effects include kyphosis, deconditioning, insomnia, and depression. Initial treatment includes bed rest, pain management with local and systemic analgesia, bracing to improve comfort, and patient reassurance. Long-term management includes spinal stretching exercises, walking, and treatment of underlying osteoporosis with calcitonin or estrogen in selected patients.
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PMID:Vertebral compression fractures: how to manage pain, avoid disability. 802 Jul 59

Amongst the spinal peptide candidates believed to be involved in the mediation of analgesia, only somatostatin fulfills the criterium of a real analgesia substance. Spinal somatostatin specifically blocks the transmission of painful stimuli. Spinal calcitonin may lower the opioid dose requirement in patients with bone metastases but it fails to relieve acute pain. The usefulness of ACTH and CRF for treatment of pain remains to be established. The role of CCK-8, vasopressin and neurotensin is unclear. The contradictory findings on antinociception using simple rodent withdrawal reflex tests (e.g. the tail flick test), or more complex behavioral tests in which supraspinal sensory processing is involved, (e.g. the hot plate test), indicate that these tests are inappropriate when neuropeptides are employed. Furthermore, due to their inability to predict analgesia in humans, they do not fulfill the guidelines proposed by the IASP that animal test procedures have to be for the benefit of humans.
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PMID:Non-opioid peptides for analgesia. 831 62

Tolerance to morphine analgesia is believed to result from a neuronal adaptation produced by continuous drug administration, although the precise mechanisms involved have yet to be established. Recently, we reported selective alterations in rat spinal calcitonin gene-related peptide (CGRP) markers in morphine-tolerant animals. In fact, increases in CGRP-like immunostaining and decrements in specific [125]hCGRP binding in the superficial laminae of the dorsal horn were correlated with the development of tolerance to the spinal antinociceptive action of morphine. Other spinally located peptides such as substance P, galanin, and neuropeptide Y were unaffected. Thus, the major goal of the present study was to investigate whether the development of tolerance to spinally infused morphine could be modulated by the blockade of dorsal horn CGRP receptors using the potent CGRP antagonist hCGRP(8-37). Indeed, cotreatments with hCGRP(8-37) prevented, in a dose-dependent manner, the development of tolerance to morphine-induced analgesia in both the rat tail-flick/tail-immersion and paw-pressure tests. Moreover, alterations in spinal CGRP markers seen in morphine-tolerant animals were not observed after a coadministration of morphine and hCGRP(8-37). These results demonstrate the existence of specific interaction between CGRP and the development of tolerance to the spinal antinociceptive effects of morphine. They also suggest that CGRP receptor antagonists could become useful adjuncts in the treatment of pain and tolerance to the antinociceptive effects of morphine.
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PMID:A calcitonin gene-related peptide receptor antagonist prevents the development of tolerance to spinal morphine analgesia. 860 14

1. The interaction of intraperitoneal administration of salmon-calcitonin with opioids was studied. The study was carried out using guinea pig ileum (mu and kappa-opioid receptors), rabbit vas deferens (kappa-opioid receptors) and mouse vas deferens (delta-opioid receptors), and selective mu, delta and kappa agonists were used in the pertinent tissues. 2. The treatment with salmon-calcitonin increased, in a dose-dependent manner, the effect of U-50,488H in guinea pig ileum and rabbit vas deferens and the effects of [D-Pen2, D-Pen5] enkephalin in mouse vas deferens. 3. The treatment with analgesic doses of salmon-calcitonin enhances the in vitro effects of kappa- and delta-opioid agonists. The increase of the effectiveness of the opioid agonists may be one of the mechanisms involved on the analgesia induced by salmon-calcitonin.
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PMID:Effect of the intraperitoneal administration of salmon-calcitonin on the "in vitro" actions of opioid agonists. 874 58

Analgesic effect of calcitonin administered in doses of 1, 3, and 5 U/100 g was studied in rats. Intrathecal administration of calcitonin (0.015 U) results in higher increase in analgesic effect compared to intraventricular injection. Intramuscular (1, 3, and 5 U/100 g) and intraventricular (0.1 U) injection of parathormone exert no analgesic effect, whereas intrathecal injection in a dose of 0.1 U resulted in statistically significant analgesia. High correlation was found for nociception and calcium level in blood. Nifedipine and isoptin (1, 5, and 10 mg/kg) were shown to reduce significantly the analgesic effect of calcitonin. On the membrane of the isolated neuron of mollusk calcitonin (10(-9) - 10(-7) M) increased and in a concentration of 10(-6) M decreased JCa. Inhibiting effect of isoptin on JCa was found for combined action of calcitonin and isoptin on the neuron membrane.
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PMID:[The effect of calcium-regulating hormones on pain sensitivity in rats]. 897 74

Clinical practice guidelines should be written for the physician who sees patients who already have or are at high risk for osteoporosis. They should also guide the physician in distinguishing between those at high and low risk and provide general guidelines for prevention of osteoporosis for the low-risk patient. Patients at high risk may require intervention to prevent further bone loss. The guidelines should be based on the strongest evidence available and be easy to comprehend and apply. Methods to identify individuals at high risk for osteoporosis must be described. Effective interventions also should be described, as should their benefits and risks. Elderly individuals who have a poor diet and little sun exposure may be vitamin D deficient unless a supplement is given. Factors that may be deleterious to the skeleton should be avoided. Weight-bearing exercise is important throughout life. Assessment of fracture risk is important in choosing candidates for intervention, especially interventions aimed at preventing osteoporosis. Measuring bone mass at any skeletal site is the necessary initial step for most individuals; measurement at the hip may best assess the risk of hip fracture. Some risk factors independent of bone mass may also aid in patient selection. The WHO has defined osteoporosis as a bone mass at least 2.5 standard deviations (SDs) below the mean of young normal. Such individuals and those with bone mass from 1 to 2.5 SDs below the mean of young normal may also be considered for intervention. The decision will depend on assessments of the risks, the costs of treatment, the desire of the patient, and the presence of other independent risk factors. The patient with an acute fracture may require an orthopedic intervention and should receive adequate analgesia. Physical therapy is an important adjunct that aids recovery. A number of therapeutic interventions, including adequate calcium intake throughout life and an adequate vitamin D intake, are available to high-risk individuals. These interventions may be recommended generally and do not require a diagnosis of osteoporosis. Similarly, a safe weight-bearing exercise program that helps to maintain muscle strength can be recommended to older patients. Other forms of therapy include hormone replacement, bisphosphonates, and calcitonin. Vitamin D analogs and selective estrogen receptor modulators may be helpful in the future. The risks and costs of each therapy should be weighed against its benefit in slowing bone loss or increasing bone mass and reducing fractures.
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PMID:Development of clinical practice guidelines for prevention and treatment of osteoporosis. 897 27

Certain types of cancer pain fail to respond well either to systemic drug therapy or to spinal opioids because of the occurrence of intolerable adverse effects. In addition to spinal opioids other drugs may produce an antinociceptive effect when administered by the spinal route, such as local anesthetics, NSAID, alpha 2-agonists, calcium-channel blockers, NMDA antagonists, cholinergic drugs, peptides such as somatostatin, octreotide or calcitonin, adenosine agonists, benzodiazepines, neurokinin and cholecystokinin antagonists, nitric oxide synthase inhibitors, corticosteroids, and enkephalinase inhibitors. All these drugs may be administered in combination between them, realising the so called balanced spinal analgesia. The aim of this study is to analyse: the available methods for the evaluation of pharmacological interactions, the types of interaction between different spinal antinociceptive drugs and the role of balanced spinal analgesia in the treatment of cancer pain. Analysis of the presented data shows that the spinal synergism between opioids-local anesthetics and opioids-alpha 2-agonists can be useful in the treatment of opioid refractory cancer pain. Furthermore, the use of cholinergic drugs combined with opioids and alpha 2-agonists may be promising. Finally, even if the synergism between NSAID or NMDA antagonists with opioids or alpha 2-agonists have been proved, at the moment their use in man by the spinal route is not advisable because of the absence of adequate studies on their neurotoxicity and adverse effects.
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PMID:[Balanced spinal analgesia in the treatment of oncologic pain. Review of the literature]. 910 86


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