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)

In 18 patients scheduled for lower intraabdominal surgery (hysterectomy), changes in thyreotropin (TSH) thyroxine (T4), triiodothyronine (T3) binding of thyroid hormones to plasma proteins (T3-uptake) and glucose in serum were evaluated. In eight patients afferent neurogenic impulses from the surgical area were blocked (Th4-S5) with bupivacaine 0.5% infused continuously into the epidural space from the start of the operation until 6 h postoperatively. All patients received general anaesthesia with thiopentone, pethidine, pancuronium and nitrous-oxide plus oxygen. The patients receiving epidural analgesia had no increase in plasma-TSH, compared to the other group, which had a significant (P less than 0.05) increase peroperatively. The patients receiving epidural analgesia were pain-free and the normal stress-induced increase in plasma-glucose was abolished. Concerning T3 we found a significant decrease in both groups and a steady level of T4- and T3-uptake without significant fluctuations. Thus it can be concluded that the effects of surgical trauma on plasma-TSH concentration are markedly similar to the effects of other anterior pituitary hormones, i.e. HGH, prolactin and ACTH.
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PMID:Per- and postoperative changes in the concentration of serum thyreotropin under general anaesthesia, compared to general anaesthesia with epidural analgesia. 359 Dec 53

Stress and pain induced by surgical trauma seem to be attenuated when calcium antagonists have been applied. In order to ascertain the effect of nimodipine, a new strong acting calcium channel blocker on plasma levels of various stress hormones twenty patients undergoing cardiovascular surgery where investigated in two groups. Ten patients received high-dose fentanyl anaesthesia (mean: 2,45 mg fentanyl/patient), whereas another ten patients were treated with 0,1 mg fentanyl/patient in addition to nimodipine 1,0 micrograms/kgbw X min (from onset of anaesthesia until start of extracorporeal circulation). Between the two groups were no significant differences with respect to perioperative course and postoperative demand for analgetics. Plasma levels of ACTH, somatotropin, glucose and free glycerol were markedly elevated in all patients (n = 20) intra- and postoperatively, whereas cortisol and prolactin remained unchanged. The present data suggest an additive analgesic effect of nimodipine during surgery. This phenomenon is possibly due to a blocking effect of calcium channel blockers on nociceptive nerves. The present model assumes that calcium is essential in pain perception and that decreased calcium would result in analgesia.
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PMID:[Calcium antagonists in anesthesia. Additive analgesia using nimodipine in heart surgery]. 408 64

The skin pain threshold was elevated significantly by weak and nonstressful acupuncture stimulation. Although an analgesic effect was obtained by acupuncture stimulation, the beta-E, ACTH, GH and TSH levels were not changed. These findings indicate that these hormone levels were not necessarily related to the skin pain threshold elevation. It is concluded therefore that an analgesic effect was induced without involving the pituitary gland by the weak acupuncture stimulation employed in our study. However, the magnitude of the stimulation may determine whether or not an analgesic effect is mediated by the pituitary gland. The possibility remains that strong acupuncture stimulation produces stress-induced analgesia (SIA). Further detailed research should be attempted.
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PMID:Effects of acupuncture anesthesia on the pituitary gland. 608 65

The effect of long term ACTH treatment on some actions of morphine were studied. The effect of ACTH administration was compared to that induced by acute dexamethasone injection. ACTH caused a delayed inhibition of the morphine induced increase in growth hormone secretion demonstrable 24 hr after the last hormone injection. The morphine induced increase of striatal DOPAC (3,4-dihydroxyphenylacetic acid) content was also inhibited by ACTH treatment, however, neither the analgesia, nor the hypermotility caused by morphine were affected. Dexamethasone did not alter significantly the responsiveness to morphine. It is concluded that the prolonged exposure to ACTH presumably causes a corticosterone-mediated loss of responsiveness of functionally restricted opiate sensitive mechanisms in the central nervous system.
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PMID:Loss of sensitivity to morphine induced by prolonged ACTH treatment. 608 72

In order to evaluate the role of endogenous opioids in sustaining analgesia induced by transcutaneous nerve stimulation (TNS), we measured plasma beta-lipotropin (BLPH), beta-endorphin (BEP), ACTH and cortisol changes concomitantly with nociceptive flexion reflex (RIII) threshold after TNS (80 microseconds rectangular waves at 85 Hz) in a group of healthy volunteers (A). The same protocol was carried out in another group of volunteers using placebo stimulation (0.5 Hz) (B). RIII threshold significantly increased 0.5 h after TNS in group A and no changes were recorded in group B. Similarly, both BLPH and BEP plasma levels increased at the end of TNS only in group A. ACTH and cortisol concentrations show only random variations after both high and low frequency TNS. A positive linear correlation was found between the maximum percentage increase of RIII threshold after high frequency TNS and the maximum percentage increase of BLPH plasma levels occurring 20 min beforehand (r = 0.856, P less than 0.001). A less positive correlation was found between RIII and BEP levels (r = 0.574, P less than 0.05). These data indicate that the so-called post-stimulation analgesia could be supported by the enhancement of the endogenous opioid system.
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PMID:Concomitant increase in nociceptive flexion reflex threshold and plasma opioids following transcutaneous nerve stimulation. 608 74

Cathinone, the active principle of Catha edulis (khat), shows long-lasting analgesic effects when the tail-flick test is used in rats. The involvement of monoamines, endogenous opioids and stress in this analgesic effect was tested. Both early (30 min) and late (24 h) analgesic effects of cathinone were prevented by reserpine or p-chlorophenylalanine, which deplete catecholamines or serotonin, respectively, and by nomifensine, which prevents neuronal uptake of biogenic amines and amphetamines. The same inhibitory effect was obtained with a high dose (4 mg/kg) of naloxone. However, rats made tolerant to morphine retained both early and late analgesic response to cathinone. The increase in plasma ACTH induced by the tail-flick test at 30 min and 24 h was significantly enhanced by cathinone, in a naloxone-reversible way. However, the analgesic responses shown at these times were not prevented by either dexamethasone or adrenalectomy. We conclude that the prolonged analgesia induced by cathinone is primarily due to an amphetamine-like activation of monoaminergic pathways, but requires the integrity of non-mu-opioid mechanisms. The involvement of the adrenohypophyseal axis in this cathinone effect is less probable.
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PMID:Prolonged analgesia induced by cathinone. The role of stress and opioid and nonopioid mechanisms. 609 60

The involvement of the endogenous analgesia systems in the mechanism of analgesia produced by electrical stimulation of the brain or resulting from certain stressful manipulations seems now well-established. The purpose of the present study was to determine whether acupuncture as a method of peripheral sensory stimulation activates, like central stimulation, the endogenous opiate system. Plasma concentrations of ACTH and the best known endogenous opiates: beta-endorphin, met- and leu-enkephalin, were determined before and after standard electroacupuncture stimulation in healthy volunteers. Acupuncture stimulation resulted in a significant (p less than 0.005) decrease of plasma beta-endorphin-like immuno-reactivity (B-EPLI), but plasma ACTH assayed did not change about 5 minutes after acupuncture. The authors conclude that the reaction of the beta-endorphin system to acupuncture (sensory peripheral) stimulation in humans did not involve pituitary hypersecretion, and suggest that the increase of beta-endorphin binding to the tissue receptor sites seems to be responsible for the peripheral (plasma) B-EPLI decrease after acupuncture.
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PMID:Plasma immunoreactive beta-endorphin and enkephalin concentration in healthy subjects before and after electroacupuncture. 613 43

The distribution of corticotropin releasing factor (CRF)-immunoreactive structures in the rat thalamus was studied after treatment with high doses of colchicine (100 micrograms/100 g b.wt.) with peroxidase-antiperoxidase (PAP) immunocytochemistry in vibratome sections. CRF-immunopositive perikarya were found in the 'posteromedial complex' of the thalamus, including the ventromedial, paracentral, mediodorsal, rhomboid, parafascicular nuclei, centrum medianum and ventromedial portion of the posterolateral nucleus. In addition, CRF-containing perikarya were observed in the pretectal and subthalamic nuclei. CRF-immunoreactive processes were seen in most of the medial nuclei of the thalamus. The presence of CRF-immunopositive structures in the thalamus suggests that CRF not only functions as a hypophysiotropic hormone regulating the release of ACTH and beta-endorphin from the pituitary, but also as a neurotransmitter or neuromodulator, playing an important role in nociception and analgesia.
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PMID:Immunocytochemical localization of corticotropin releasing factor (CRF)-like immunoreactivity in the thalamus of the rat. 615 62

New data on tachykinins and bombesins are displayed and the present situation of research on the novel amphibian skin peptides sauvagine and dermorphin is illustrated. The potent stimulant effect of sauvagine on ACTH and beta-endorphin release has been confirmed both in vivo and on columns of isolated and dispersed rat pituitary cells, and similarly the potent inhibitory effect on PRL and GH release, both in the rat and man. Particular emphasis is laid on the occurrence of sauvagine-like immunoreactivity in fish urophysis and in amphibian nervous structures, including the retina. It is suggested that the long-searched corticotropin releasing factor and PRL release-inhibiting factor may be a sauvagine-like peptide. Dermorphin, in its turn, has been found to cause, by intracerebroventricular injection, not only analgesia and catalepsy, but also conspicuous EEG and behavioral changes in the rabbit and chick, as well as a sharp reduction in gastric emptying time and gastric acid output in the rat, together with marked stimulation of PRL release.
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PMID:The brain-gut-skin triangle: new peptides. 617 95

The present paper examines the role of pituitary pools of beta-endorphin in mediating the elevation in nociceptive threshold produced by stress. A 5 min foot-shock stress, characterized as activating both central and pituitary systems of beta-endorphin (beta-EP) and eliciting a naloxone-attenuated elevation in tail-flick latency in rats, was employed. Both total hypophysectomy and selective ablation of the anterior lobe almost completely abolished stress-induced analgesia (SIA), whereas removal of the neuro-intermediate lobe alone proved ineffective. However, manipulation of the hypothalamus-pituitary-adrenal feedback system by administration of either the corticosteroid, dexamethasone, or the corticosteroid synthesis inhibitor, metyrapone, in neither case affected SIA. None of these surgical or pharmacological manoeuvres affected basal nociceptive threshold (BNT). These data indicate that although the integrity of the adenohypophysis is essential for the manifestation of SIA, an adenohypophyseal mechanism, probably involving neither ACTH nor beta-EP, is essential for the development of the analgesia which accompanies stress.
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PMID:A non-beta-endorphinergic adenohypophyseal mechanism is essential for an analgetic response to stress. 625 Jan 16


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