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)

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 major objective of these experiments was to determine long-term effects on the hypothalamic-pituitary adrenal axis (HPAA) of adult rats exposed during development to chlordecone, an organochlorine insecticide. Chlordecone was administered to mothers prenatally plus the first 12 days of the neonatal period (6 ppm in the diet) or neonatally via a single subcutaneous injection to rats at 4 days of age (1 mg/pup in 20 micrograms of DMSO). DMSO (20 microliters/pup) and dexamethasone (100 micrograms/pup in 20 microliters saline) were also injected on day 4. HPAA function was evaluated at 70-80 days of age. Responsiveness of the HPAA to a repeated stressor was evaluated by exposing rats of each treatment group to a 7-day stress-induced analgesia (SIA) paradigm consisting of a daily 15 sec foot-shock (0.9 mA) exposure which was preceded by a 15 sec white noise conditioned stimulus. The behavioral response to daily stress was evaluated by measuring tail-flick latencies immediately before and/or after each stress exposure. The conditioned response to stress was evaluated 24 hours after the last of 7 daily foot-shock sessions in which rats of each treatment and experimental group were exposed to the shock chamber only. All rats were killed 15 minutes after the final session and tissue (serum and adrenals) were removed and frozen for later chemical analysis; serum and adrenal corticosterone (CS) and serum prolactin (Prl) levels were measured. Perinatal exposure to chlordecone did not significantly alter the behavioral and/or neuroendocrine responses to stress. Ambient hormone levels (both CS and Prl), however, were uniformly attenuated by chlordecone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothalamic-pituitary adrenal (HPAA) axis function in adult Fischer-344 rats exposed during development to neurotoxic chemicals perinatally. 608 62

The effects of two different concentrations of halothane (0.5 or 1.5%) and two different doses of thiopentone (4.5 or 10 mg kg-1) on the plasma concentrations of cortisol, growth hormone (GH) and prolactin (PRL) were studied in response to the stress of tracheal intubation. Additionally, the effect of the intratracheal administration of 4% lignocaine spray 2 ml was investigated. The study group included 48 healthy women. During a "light" level of halothane and thiopentone anaesthesia, the plasma concentration of cortisol increased in response to tracheal intubation in the patients who did not receive intratracheal analgesia. Topical analgesia with lignocaine prevented the increase in cortisol concentration and this would seem to indicate that the increase was caused by the stress of laryngoscopy and intubation. At a deeper level of halothane anaesthesia, and in association with the larger dose of thiopentone the increase in cortisol concentration was suppressed. GH did not change from the preanaesthetic value in any group and there were no differences between the control group and the study groups. PRL increased significantly in all groups. Increasing the dose of thiopentone caused a further increase in PRL concentration which indicated a direct stimulatory action of thiopentone on PRL release.
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PMID:Modification of aspects of the endocrine response to tracheal intubation by lignocaine, halothane and thiopentone. 623 Oct 43

Tiapride, a substituted benzamide, exerts an antalgic effect in man. To examine the possibility that tiapride analgesia might be related to a mechanism involving a release of endogenous opioids, the acute effects of an intravenous injection of the drug on plasma radioimmunoassayable beta-endorphin were studied in patients with pain from cancer (placebo-tiapride double-blind randomized trial). Seeing that substituted benzamides affect prolactin secretion, the plasmatic levels of prolactin and dopamine, a known factor inhibiting prolactin release, were studied as well. The tiapride infusion produced a slight but significant increase in plasma beta-endorphin level, an early and significant increase in plasma prolactin, and a sudden and highly significant decrease in plasma dopamine. These results are compatible with the hypothesis that tiapride influences the neuroendocrine system.
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PMID:Effects of tiapride infusion on plasma levels of beta-endorphin, prolactin and dopamine in patients with pain from cancer. 626 2

Tiapride, a substituted benzamide, exerts an antalgic effect in man. To examine the possibility that tiapride analgesia might be related to a mechanism involving a release of endogenous opioids, the acute effects of an intravenous injection of the drug on plasma radioimmunoassayable beta-endorphin were studied in patients with pain from cancer (placebo-tiapride double-blind randomized trial). Seeing that substituted benzamides affect prolactin secretion, the plasmatic levels of prolactin and dopamine, a known factor inhibiting prolactin release, were studied as well. The tiapride infusion produced a slight but significant increase in plasma beta-endorphin level, an early and significant increase in plasma prolactin, and a sudden and highly significant decrease in plasma dopamine. These results are compatible with the hypothesis that tiapride influences the neuroendocrine system.
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PMID:[Effects of tiapride infusion on plasma levels of beta-endorphin, prolactin and dopamine in patients with pain from cancer (author's transl)]. 626 92

The dental pain threshold elevation produced by non-painful, low-frequency transcutaneous electrical nerve stimulation (TENS) in healthy humans was not reduced by the administration of 0.8 mg of naloxone i.v. Neither ACTH, prolactin nor growth hormone (GH) release were related to the pain threshold elevations. The present study indicates that the dental pain threshold elevation during non-painful, low-frequency TENS is not based on the same opioid-dependent mechanisms as the dental pain threshold elevation during acupuncture or the clinical analgesia during low-frequency TENS. Stress or other adenohypophyseal mechanisms involving ACTH, prolactin or GH do not explain the analgesia induced by non-painful, low-frequency TENS.
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PMID:Dental analgesia produced by non-painful low-frequency stimulation is not influenced by stress or reversed by naloxone. 629 Sep 63

Morphine has a variety of actions on the release of pituitary hormones in addition to its analgesic actions. In the rat, morphine releases prolactin and growth hormone at doses comparable to those active in the tailflick analgesic assay. Naloxazone selectively inhibits the high affinity (mu 1) binding site and dramatically decreases morphine's analgesic potency for over 24 hours. In an effort to determine the opiate receptor mechanisms of morphine-induced prolactin and growth hormone release, groups of rats were treated with either naloxone or naloxazone and 24 hours later the prolactin and growth hormone response to morphine sulfate determined. Peak prolactin levels in the group treated the previous day with naloxone were very similar to levels in untreated controls. However, the peak prolactin levels in the group that received naloxazone the day before were depressed 80% (p less than 0.005). By contrast, growth hormone levels in the naloxazone-treated animals were actually higher than in the naloxone-treated group. Thus prolactin release, like analgesia, appears to be mediated through high affinity, or mu 1, sites, while growth hormone release is not.
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PMID:Different receptors mediate morphine-induced prolactin and growth hormone release. 629 16

Opiate receptors in the central nervous system may be classified according to pharmacological, behavioural, or binding studies. Classical mu-receptors probably have beta-endorphin as an endogenous ligand, and seem to be involved in the modulation of pain perception, low-frequency acupuncture analgesia, and the stimulation of prolactin, growth hormone and thyroid-stimulating hormone release. Met-enkephalin is likely to be an endogenous ligand for the delta-receptors, which predominate in the basal ganglia and limbic systems; such receptors may tonically inhibit the release of corticotrophin-releasing factor. It has been suggested that the newly-described kappa-receptors may inhibit the release of vasopressin and gonadotrophin-releasing factor; dynorphin may be their endogenous ligand. Endogenous opiates controlling cardiovascular and respiratory reflexes are likely to activate mu-receptors, while high-frequency acupuncture may alleviate the symptoms of opiate withdrawal by allowing an increase in Met-enkephalin to activate delta-receptors. In the periphery, beta-endorphin is concentrated in the corticotrophs of the anterior pituitary, and is cosecreted with ACTH and related peptides. Circulating Met-enkephalin originates in the gut, sympathetic nervous system and adrenal medulla. Met-enkephalin may also be extracted from carcinoid tumours and phaeochromocytomas. Elevations in circulating Met-enkephalin may occur in certain disease states with cardiovascular and psychiatric manifestations. However, manipulation of endogenous or exogenous opiates has as yet no certain place in any clinical situation.
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PMID:Opiate receptors: enkephalins and endorphins. 630 48

Endogenous hyperprolactinaemia induced by anterior pituitary transplantation under the kidney capsule has been found to reduce the behavioural responsiveness to electrical footshock and to increase morphine-induced analgesia. The apparent analgesic effect of prolactin has been related to the stimulation of nigro-striatal dopaminergic transmission, as suggested by the increase in striatal dopamine turnover observed in hyperprolactinaemic rats. It seems likely that central opiate system is involved in the behavioural effects of prolactin. Thus, naloxone prevents the effects of hyperprolactinaemia on footshock responsiveness and heroin self-administration is decreased in hyperprolactinaemic rats.
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PMID:Role of prolactin-opiate interactions in the central regulation of pain threshold. 631 24

Evidence from a variety of experimental models has suggested the existence of mu 1, mu 2 and delta binding sites for morphine and the enkephalins in the central nervous system. Additional biochemical experiments now support this concept of a common high affinity site for opiates and opioid peptides. Mu sites have now been implicated in a number of pharmacological actions, including supraspinal analgesia, prolactin release, and catalepsy, but not in others (spinal analgesia, respiratory depression, and the guinea pig ileum). The hypothesis of mu 1 sites was supported by the unique opioid meptazinol, which selectively bound to mu 1 sites. As expected from its mu 1 binding selectivity, its analgesic actions in the mouse, localized supraspinally, were antagonized by the selective mu 1 antagonist naloxonazine and it had no respiratory depressant actions. Other binding studies suggested the presence of discrete SKF10,047-selective (KD approximately 5 nM) binding sites in rat brain which differed from both kappa sites and the previously reported PCP-binding sigma sites. Additional binding and autoradiographical studies have also implied the presence of beta-endorphin, or epsilon, sites in the CNS.
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PMID:Biochemical and pharmacological evidence for opioid receptor multiplicity in the central nervous system. 631 56


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