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 effect of dexamethasone on exercise-induced adrenocorticotropin (ACTH) secretion and dental analgesia was studied in healthy human subjects. Different levels of exercise (100-200 W) were produced by a cycle ergometer. Dental pain thresholds were tested with a constant current stimulator. Dental pain thresholds were elevated with increasing work loads, and the elevation was still significant 30 min after the end of the exercise. Dexamethasone produced a significant reversal of exercise-induced pain threshold elevations concomitantly with the suppression of exercise-induced ACTH release. The results suggest that the corticotropin releasing factor-ACTH axis is involved in the exercise-induced analgesia.
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PMID:Dexamethasone attenuates exercise-induced dental analgesia in man. 216 84

The effects of ip intra-PAG injection of ACTH on serotonin (5-HT), norepinephrine (NE) contents of hippocampus and hypothalamus and pain threshold were investigated. The results showed: (1) After ip ACTH, the pain threshold, the contents of 5-HT of the two brain regions and the NE content of hippocampus were markedly elevated. Prior destruction of periaqueductal gray (PAG), the elevation of pain threshold and the increase of the 5-HT contents of two brain regions due to ip ACTH were completely abolished, while the effect of ACTH in elevating NE content of hippocampus still persisted. (2) After intra-PAG injection of ACTH, the pain threshold and the 5-HT contents in hippocampus and hypothalamus were significantly increased, however, the NE levels in hippocampus and hypothalamus showed no significant changes. The analgesic effect of the intra-PAG injection of ACTH was prevented by icv LSD, but not by naloxone, atropine, hexamethonium and phentolamine. (3) After icv ACTH, the pain threshold did not change. These results suggest that the serotoninergic system may be activated by PAG for mediation of ACTH-induced analgesia.
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PMID:[Serotonin of hippocampus and hypothalamus taking part in the analgesic effect of adrenocorticotropic hormone in rats]. 216 93

Conjugate of horseradish peroxidase and wheat germ agglutinin (HRP-WGA conjugate) was injected into the midbrain central gray (MCG) of three adult rats. Frontal sections of the diencephalon were first treated with diaminobenzidine and hydrogen peroxide to detect the retrogradely transported conjugate. They were then stained immunohistochemically to detect pro-opiomelanocortin (POMC)-derived peptides (ACTH, beta-endorphin and alpha-MSH). The coexistence of the three POMC-derived peptides was confirmed by the immunohistochemistry of three consecutive sections stained with antiserum specific to each peptide. Some of the neuronal perikarya distributed in and around the arcuate nucleus were positive to the immunohistochemical stain for POMC-derived peptides, and, concomitantly, were labeled with HRP-WGA conjugate, which indicated that they projected to the MCG. They were mostly concentrated in the rostral three-fifths of the arcuate nucleus. The finding that some of the POMC neurons in the arcuate nucleus project to the midbrain central gray deserves interest, because the central gray is involved in analgesia induced by opioid peptides.
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PMID:Projection of pro-opiomelanocortin neurons from the rat arcuate nucleus to the midbrain central gray as demonstrated by double staining with retrograde labeling and immunohistochemistry. 245 87

Prolactin, ACTH, cortisol and HGH levels have been studied on 30 pregnant women in three different periods: during the labour, at the delivery and 24 hours later. They were divided into 3 groups depending on the analgesia: I) no analgesia (n = 10); II) psychoprophylaxis (n = 10), and III) extradural analgesia (n = 10). Prolactin levels increased during delivery and 24 hours later. A significant increase of ACTH levels (p less than 0.01) was observed during the delivery in the 3 groups even though they were under hasal values 24 hours later. Cortisol increased 38% (p less than 0.01) and 52% (p less than 0.02) in II and III groups, respectively during the delivery. No difference was found with HGH. Our results suggest that endocrine response modified by labour and delivery doesn't change with different analgesia techniques.
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PMID:[Eutopic parturition: psychoprophylaxis or extradural analgesia. Influence on the endocrine response]. 255 43

In this study we have examined the results of salmon calcitonin treatment on migraine pain. The mechanism by which calcitonin induces analgesia is still not understood. We observed the effect of a 5-day treatment with salmon calcitonin (IM 100 IU/day) on circulating levels of beta-endorphin, ACTH, and cortisol in 20 patients with migraine during the headache-free period. All 3 hormones were increased after the calcitonin administration and the maximum increase was obtained in beta-endorphin levels. There were significant statistical correlations between beta-endorphin, ACTH, and cortisol levels determined before and after calcitonin treatment.
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PMID:Treatment of migraine with salmon calcitonin: effects on plasma beta-endorphin, ACTH and cortisol levels. 256 Apr 8

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

Evidence suggests a close relationship between ACTH and opioids. They are derived from the same precursor molecule, released concomitantly in response to stress and are known to interact at receptor level. Acute exposure to endogenous opioids induces analgesia in the short-term yet shifts the morphine dose-response curve to the right for a period of several weeks. Therefore, the possibility exists that ACTH might also exert an influence extending beyond that suggested by its biological half-life. To investigate this further, DBA/2 mice were pretreated with porcine ACTH left undisturbed for 3 days, then challenged with morphine. Dose-response studies indicated that pretreatment with 10 but not 0, 0.1 or 1.0 IU ACTH influenced responsivity to morphine, rendering a sub-analgesic dose (1.0 mg/kg) effective and significantly enhancing the degree of analgesia observed following treatment with 5 mg/kg morphine, suggesting a shift in the dose-response curve to the left. Time-course analysis revealed 5 mg/kg morphine to induce an analgesic reaction with an onset of between 15-30 and lasting between 60 and 120 min post opiate administration. ACTH pretreatment did not influence this time course, however a significantly greater degree of analgesia was observed at 60 min post morphine injection in 10 IU ACTH pretreated animals than in saline pretreated controls. ACTH pretreatment further influenced subsequent responding to chronic morphine administration. Whilst saline pretreated animals demonstrated significant analgesia in response to the first administration, tolerance to this effect had developed following four days of repeated exposure to morphine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACTH: a single pretreatment enhances the analgesic efficacy of and prevents the development of tolerance to morphine. 283 53

The purpose of the present study was to assess the repercussion of morphine injected in the intrathecal space on postoperative neuroendocrine response and the correlation with pain relief in the postop period. We studied 50 healthy patients (ASA I-II) submitted to orthopaedic surgery under general anaesthesia (N = 25) or spinal anaesthesia (N = 25). In the group under general anaesthesia we observed a hypersecretion of ADH, ACTH, cortisol and aldosterone during and after surgery. In the group un spinal anaesthesia, it was evident, on the contrary, a blockade of the neuroendocrine response during surgery, as well as an attenuation during postoperative period. Intraoperative and postoperative bleeding with spinal anaesthesia was significantly lower (p less than 0.01; p less than 0.05 respectively) than with general anaesthesia. Postoperative analgesia was excellent in group with spinal anaesthesia; the average duration of analgesia was 16.3 hours. We conclude that small intrathecal doses of morphine have beneficial effects and may be used usefulness in orthopaedic surgery.
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PMID:[A bupivacaine-morphine combination by intrathecal route: correlation between pain relief and postoperative neuroendocrine response]. 285 85

An acute form of "stress-analgesia" is evoked by allowing the smoke of a cigarette to envelope the nostrils of unanaesthetized rabbits. The response consists of an immediate and generalized arrest of spontaneous movements, including respiration and expiration, reduced muscular tone, and unresponsiveness to pinching. This motor "paralysis" is accompanied by a profound bradycardia. Attempts have been made to identify the neurotransmitters involved in "the smoke reflex" by the intervention of antagonists and psychopharmaca. The bradycardia was selectively blocked by atropine, leaving the somatomotor inhibition unaltered. All components of the response were abolished by approximately 60% by clonidine and by 40% by the tricyclic antidepressant amitriptyline, both of which are known to attenuate the release of noradrenaline as agonsits of alpha 2-adrenoceptors. Yohimbine blocked the clonidine effect. Naloxone (1-2 mg/kg), p-chlorphenylalanine and dexamethasone failed to influence the reflex response, suggesting that opiate, serotonergic and ACTH-systems do not play a critical role. The same applied to the benzodiazepine chlordiapoxide. The results suggest that this acute stress-induced analgesia is mediated via a noradrenergic system. The relationship of the smoke reflex to "the fear paralysis reflex", a possible trigger mechanism for the sudden infant death syndrome, is discussed.
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PMID:Neurotransmitters in "the smoke reflex" in rabbits. 288 36

Effects of electroacupuncture (EA) on pain threshold and beta-endorphin (beta-End) contents in plasma, pituitary (Pit), hypothalamus (Hyp) and cerebrospinal fluid (CSF) were studied in nontreated, dexamethasone (Dex) treated and adrenalectomized (Adrex) male SD rats by the use of specific determination of rat beta-End (combination of HPLC and RIA). EA increased pain threshold and plasma beta-End with no effect on beta-End contents in Pit, Hyp and CSF. Dex did not affect control pain threshold, but tended to reduce EA-induced increase in pain threshold (EA-analgesia, EAA) and EA-induced increase in plasma beta-End. Adrex increased plasma beta-End without change in control pain threshold. Adrex tended to reduce EAA, but a tendency of further increase in plasma beta-End was observed after addition of EA. Adrex increased Pit beta-End, but no further change in Pit beta-End was observed after addition of EA. A positive correlation between plasma beta-End and plasma ACTH was observed in nontreated, Dex treated and Adrex rats. No correlation between plasma beta-End and potency of EAA was observed in nontreated, Dex treated and Adrex rats. The hind-paw pressure test without EA increased plasma beta-End to the same degree as that produced by EA, and it produced no analgesia. These results suggest that Pit beta-End may not be mainly involved in the development of EAA.
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PMID:[Effects of electroacupuncture on beta-endorphin contents in rats]. 293 79


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