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)

A marked expression of the c-fos proto-oncogene has been recently reported in cells of the anterior lobe of the pituitary gland in rats subject to electroacupuncture or noxious thermal stimulation under pentobarbital anaesthesia. The present study was undertaken to identify the activated pituitary cells. Following both kinds of stimulation, most Fos-immunoreactive anterior lobe cells showed colocalization with adrenocorticotropic hormone or beta-endorphin immunoreactivity. No c-fos expression occurred in pituitary cells immunoreactive for growth hormone, prolactin, luteinizing hormone, or thyrotropin-stimulating hormone. A marked rise of adrenocorticotropic hormone and beta-endorphin concentrations occurred in plasma. In the hypothalamus, c-fos expression was increased in the mediobasal nuclei-namely, the arcuate nucleus-and in the paraventricular nucleus, but more in the former. It is suggested that somatosensory noxious input, or the partly noxious input evoked by electroacupuncture, activate the hypothalamo-pituitary-adrenocortical axis as in common forms of stress, but with a specific activation of the mediobasal hypothalamic nuclei and no stimulation of intermediate lobe cells. Opiate release from the pituitary gland may contribute to acupuncture analgesia or the intrinsic antinociceptive reactions triggered by noxious stimulation.
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PMID:Activation of anterior lobe corticotrophs by electroacupuncture or noxious stimulation in the anaesthetized rat, as shown by colocalization of Fos protein with ACTH and beta-endorphin and increased hormone release. 873 78

This paper presents a historical overview of melanocortin (MC) research from the early investigations of the many noncorticotropic effects of peptide fragments of adrenocorticotropic hormone to the present focus on the discovery and cloning of the MC receptors (MCRs). Final acceptance of the passage of neuropeptides through the blood-brain barrier provided the scientific basis for the neuropeptide concept, formulated previously by both De Weid and Kastin, that peripherally administered neuropeptides affect neural processes. The discussion includes melanocortin effects on behavior, the cardiovascular system, central and peripheral electrophysiological parameters, food intake, inflammation and analgesia, nerve regeneration and neuroprotection, and development. The localization of specific MCRs in both neural and nonneural tissues is correlated with the pleiotropic effects discussed.
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PMID:New vistas for melanocortins. Finally, an explanation for their pleiotropic functions. 1067 31

Experiments on anaesthetized male Sprague-Dawley rats were performed to study the effects of adrenocorticotropic hormone (ACTH) on pain sensitivity. Systemic administration of ACTH to animals with normal hormone production induced rapidly developing (starting at 3 min) and prolonged (30 min) increases in pain response thresholds. Blockade of opiate receptors led to suppression of the initial stage of the analgesic effect of ACTH: the response was seen only from 15 to 30 min. In animals with deficient glucocorticoid production, the duration of the analgesic action of ACTH decreased to 15 min. Analgesia was completely eliminated by the combination of suppression of glucocorticoid production and blockade of opiate receptors. The analgesic effect of ACTH was mediated by two mechanisms: 1) a rapidly-acting (from 3 to 15 min) mechanism associated with opiate receptors and not related to glucocorticoids, and 2) a delayed (from 15 to 30 min) mechanism associated with glucocorticoids but not opiate receptors.
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PMID:Mechanisms of the effects of adrenocorticotropic hormone on pain sensitivity in rats. 1463 95

Experiments on conscious male Sprague-Dawley rats were performed to study the effects of adrenocorticotropic hormone (ACTH) on pain reactions. Pain sensitivity was assessed in terms of the latent period of tail withdrawal in response to heat. Systemic administration of ACTH and glucocorticoids to animals with normal levels of hormone production led to increases in the latent period of the tailflick reaction. The roles of glucocorticoids and opioid peptides in ACTH-induced analgesia were addressed in experiment on animals with deficient glucocorticoid production and animals in which opiate receptors were blocked with naltrexone. Deficiency in glucocorticoid production had no effect on ACTH-induced increases in the latent period of the tailflick reaction, while blockade of opiate receptors completely eliminated this effect of ACTH. ACTH-induced analgesia in conscious rats is mediated by opiate receptors and not by glucocorticoids.
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PMID:The role of adrenocorticotropic hormone in the inhibition of pain reactions in conscious rats. 1536 3

We studied the effect of large-dose intrathecal sufentanil (ITS) for major abdominal surgery on the hormonal stress response. Forty patients were randomly allocated to receive either IV sufentanil (IVS) or 150 microg of ITS as part of general anesthesia. In the IVS group, adrenocorticotropic hormone (ACTH) and cortisol concentrations were larger than baseline and the ITS group, 60 min after incision and at skin closure. Plasma concentrations of cortisol and ACTH were not different from baseline in the ITS group during surgery. Six hours after skin closure, cortisol concentrations were larger than baseline in both groups. Twenty-four and 48 h after skin closure, ACTH and cortisol values were similar between groups. Norepinephrine concentrations increased after surgery in both groups. Blood glucose levels increased in both groups during and after surgery. Pain scores and morphine consumption during the first 48 h after surgery were lower in the ITS group. The data show that large-dose ITS prevents the intraoperative hormonal stress response in comparison with balanced anesthesia. We speculate that this is due to the highly specific binding of sufentanil to spinal and supraspinal receptors. This technique improves postoperative analgesia when compared with balanced anesthesia.
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PMID:Large-dose intrathecal sufentanil prevents the hormonal stress response during major abdominal surgery: a comparison with intravenous sufentanil in a prospective randomized trial. 1538 60

Surgical stress may cause neural, endocrine, metabolic and humoral responses depending on the severity of the procedure. In this study, we aimed to study the effect of the preoperatively given ascorbic acid (AA), which is an antioxidant, and its role in the biosynthesis of neuropituitary hormones on the surgical stress response. Twenty-two American Society of Anaesthesiologists I and II patients ageing between 18 and 40, who have no endocrine and metabolic disease, and undergoing abdominal operation for non-malignant diseases were allocated to the study. These non-premedicated patients were divided into two groups in random: Group I, etomidate group; and Group II, AA plus etomidate group. AA was given to patients in Group II 20min before etomidate injection. After monitoring the patient, anaesthetic induction was applied by giving 0.3 mg/kg of etomidate, 2 microg/kg of fentanyl and 0.1 mg/kg of vecuronium. Anaesthesia was continued with 1-0.7% isoflurane and N2O/O2 (67 and 37%, respectively). Tramadol was given for the management of post-operative analgesia. Blood samples were obtained from all patients before the operation and at second, sixth, twelfth and twenty-forth hours after the beginning of operation for cortisol, adrenocorticotropic hormone (ACTH), osteocalcin, insulin and blood glucose level analyses. There was no statistically significant difference in cortisol, osteocalcin, insulin and glucose levels in both groups, when compared to the control levels. Whereas, patients in Group II had higher levels of cortisol than the control group at sixth hour, which were in normal limits, and there was no decrease in osteocalcin concentration. ACTH level was increased at the second and sixth hours, which was statistically significant, but at twelfth and twenty-forth hours, they were close to control group levels. As a result, we conclude that AA given before anaesthesia achieved by etomidate is not sufficient for the prevention of surgical stress response and that AA induction before anaesthesia should be preferred, particularly for the prevention of decrease in osteocalcin levels.
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PMID:Effect of ascorbic acid on surgical stress response in gynecologic surgery. 1558 71

Exposure to stress triggers hormonal and behavioral responses. It has been shown that the endogenous opioid system plays a role in some physiological reactions to stress. The opioid system was described to mediate analgesia induced by mild stressors and to modulate the activation of the hypothalamic-pituitary-adrenal axis. Our study assessed the contribution of opioid receptors in stress-induced analgesia and adrenocorticotropic hormone (ACTH) and corticosterone release by a genetic approach. We performed a parallel analysis of mice deficient in mu, delta, or kappa opioid receptors, as well as of triple opioid receptor knockout mice, following exposure to a mild stress (3-min swim at 32 degrees C). In wild-type mice, stress elicited an increase in jumping latency on the hot plate, which was influenced by gender and genetic background. This analgesic response was reversed both by naloxone and by the triple mutation, and decreased in mu and delta opioid receptor knockout females. In wild-type females, stress also delayed front- and hindpaw behaviors in the hot plate test and increased tail-flick latency in the tail immersion test. Opioid receptor deletion however did not affect these stress responses. In addition, stress produced an increase in ACTH and corticosterone plasma levels. This endocrine response remained unchanged in all mutant strains. Therefore our data indicate that, under our stress conditions, the endogenous opioid system is recruited to produce some analgesia whereas it does not influence hypothalamic-pituitary-adrenal axis activity. This implies that brain circuits mediating analgesic and hormonal responses to stress can be dissociated.
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PMID:Dissociation of analgesic and hormonal responses to forced swim stress using opioid receptor knockout mice. 1623 85

We investigated whether perioperative extensive epidural block (C3-L) affects postoperative immune response in patients undergoing radical esophagectomy. Patients undergoing radical esophagectomy were randomly assigned to either general anesthesia with continuous epidural infusion via 2 epidural catheters that was continued for postoperative analgesia (group E, n = 15) or intraoperative general anesthesia and postoperative IV morphine analgesia (group G, n = 15). Plasma levels of stress hormones, cytokines, C-reactive protein (CRP), leukocyte counts, and distribution of lymphocyte subsets were assessed before and after surgery and on postoperative days (PODs) 1 and 3. In comparison with group E, significant increases in plasma epinephrine level at the end of surgery (P < 0.05) and norepinephrine level at the end of surgery (P < 0.01) and on POD1 (P < 0.01) and POD3 (P < 0.01) and significant decrease in cluster of differentiation (CD4/CD8 ratio) at the end of surgery (P < 0.05) were observed in group G. However, there were no significant differences in other variables between groups. In both groups, plasma cortisol, adrenocorticotropic hormone, interleukin (IL)-1beta, IL-6, IL-10, and CRP levels were increased after surgery (each group P < 0.01) and IL-1beta, IL-6, IL-10, and CRP were still increased on POD1 and POD3 (each change, each group P < 0.01). Leukocyte counts were increased on POD1 (each group P < 0.05) and POD3 (each group P < 0.01). The proportion of lymphocytes decreased from the end of surgery to POD3 (each group P < 0.01). The proportion of B cells was increased on POD1 (each group P < 0.01); that of natural killer cells was decreased at POD1 and POD3 (each group P < 0.01). We conclude that tissue damage and inflammation apparently overcome the effects of extensive epidural block on stress response and immune function in radical esophagectomy.
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PMID:The effects of continuous epidural anesthesia and analgesia on stress response and immune function in patients undergoing radical esophagectomy. 1624 24

Despite the increasing research on placebos in recent times, little is known about the nocebo effect, a phenomenon that is opposite to the placebo effect and whereby expectations of symptom worsening play a crucial role. By studying experimental ischemic arm pain in healthy volunteers and by using a neuropharmacological approach, we found that verbally induced nocebo hyperalgesia was associated to hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, as assessed by means of adrenocorticotropic hormone and cortisol plasma concentrations. Both nocebo hyperalgesia and HPA hyperactivity were antagonized by the benzodiazepine diazepam, suggesting that anxiety played a major role in these effects. The administration of the mixed cholecystokinin (CCK) type-A/B receptor antagonist proglumide blocked nocebo hyperalgesia completely but had no effect on HPA hyperactivity, which suggests a specific involvement of CCK in the hyperalgesic but not in the anxiety component of the nocebo effect. Importantly, both diazepam and proglumide did not show analgesic properties on basal pain, because they acted only on the nocebo-induced pain increase. These data indicate a close relationship between anxiety and nocebo hyperalgesia, in which the CCKergic systems play a key role in anxiety-induced hyperalgesia. These results, together with previous findings showing that placebo analgesia is mediated by endogenous opioids, suggest that the analgesic placebo/hyperalgesic nocebo phenomenon may involve the opposite activation of endogenous opioidergic and CCKergic systems.
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PMID:The biochemical and neuroendocrine bases of the hyperalgesic nocebo effect. 1710 75

1. Studies, using a wide variety of stressors, have clearly indicated that the pattern of neuroendocrine response is dependent upon the stress stimulus applied. 2. The Tyr-MIF-1 family of peptides (Tyr-MIF-1s) includes MIF-1, Tyr-MIF-1, Tyr-W-MIF-1 and Tyr-K-MIF-1. These neuropeptides, neuromodulators are able to inhibit the expression of some forms of stress-induced analgesia. 3. The aim of this study was to compare changes in ACTH and corticosterone (CORT) concentration after various stressors (immobilization, cold and heat), as well as after injection of investigated Tyr-MIF-1s peptides. 4. According to our results, hypothalamic-pituitary-adrenal (HPA) system was activated by all the stressors applied. Heat and immobilization are stronger stressors, as the exposure of animals to a high ambient temperature and immobilization resulted in the highest rise of plasma ACTH and CORT concentration when compared with cold stress. Moreover, all the investigated peptides from Tyr-MIF-1 family, administered after application of stressors, inhibited the elevations in adrenocorticotropic hormone (ACTH) and corticosterone (CORT) plasma concentrations significantly. 5. In conclusion, the various stressors applied seem to induce a different response of the HPA system as judged by quantitative changes in ACTH and CORT release. We suggest that Tyr-MIF-1 peptides may possess anti-stressor effects, as they inhibited stress-induced rising in two hormones that were investigated.
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PMID:Effect of Tyr-MIF-1 peptides on blood ACTH and corticosterone concentration induced by three experimental models of stress. 1879 7


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