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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet MAO activity was investigated in 32 healthy volunteers and 22 patients with chronic pain syndrome. The MAO activity did not differ between the healthy volunteers and the pain patients. There was a tendency for patients with low platelet MAO activity to have somewhat longer pain duration and somewhat higher pain levels but the difference was not statistically significant. Patients with low platelet MAO activity were found to have higher values on the Zuckerman sensation seeking scale, a disturbed diurnal pattern of plasma cortisol and a tendency towards lower concentrations of endorphins in CSF. It is postulated that platelet MAO activity reflects the activity of the serotoninergic part of the serotonin--ACTH--cortisol system.
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PMID:Platelet MAO activity in patients with chronic pain syndrome. Relationship to personality traits, endorphins in CSF and plasma cortisol. 687 94

We have seen that exposure of an organism to any of a wide range of stressful situations can induce alterations in sensitivity to pain that outlast the exposure. Not all stressors induce analgesia; among those that do not are some that produce maximal elevations in plasma beta-endorphin, ACTH, and adrenal corticosteroids. Some examples of SIA are sensitive to opiate receptor blockade by naloxone, but others are not. Hypophysectomy produces a similarly uneven profile of effects across different stressors. This diversity has often been interpreted as evidence for the existence of an array of pain inhibitory systems, with differing physiological properties and activated by different stressors. However, it might also suggest that stressors can prompt a variety of behavioral changes, many of which can be interpreted as analgesia if a pain reflex test is employed as the dependent measure.
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PMID:The role of endorphins in stress-induced analgesia. 696 59

Experiments on male rats were carried out. Prolonged emotional stress was produced by periodic pain stimulation with a weak electric current. Examination of 11-hydroxycorticosteroids (11-HOCS) in the blood and tissue levels has shown an increase in the concentration of total and free 11-HOCS during the first 30 days. By the 130th day 11-HOCS content abruptly fell in the blood and tissues despite the fact that the reserve potentialities of the adrenal cortex (ACTH test) were within normal. On the contrary, the catecholamine concentration in the animals' urine sharply rose by the end of the experiments.
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PMID:[Dynamics of the change in the level of corticosteroids in the blood and tissues and of catecholamines in the urine of rats in the process of developing an adaptation reaction to emotional stress]. 719 98

Early evidence has indicated the presence and involvement of specific neural systems which can inhibit the responses to painful stimuli. More recently, further advances suggest that the opiate system may interact with other systems to modulate the analgesia produced by the opiates or various stressors. Since corticosteroids were found to be elevated under the conditions of different stress-induced analgesia (SIA), there may be interactions between the pain-inhibiting systems and the corticosteroids. Recently it was reported that acute stress or long-term adrenalectomy can result in release of beta-endorphin (beta E) and ACTH from the pituitary gland, which can be blocked by dexamethasone. In our early studies we have shown partial antagonism of the SIA by dexamethasone and complete antagonism after naloxone. In this report it was found that chronic treatment of the rats with 0.02% metyrapone in drinking water for 8 weeks resulted in minor hyperalgesia. The chronic pretreatment with metyrapone resulted in a significant potentiation of the analgesia induced via the cold swim stress model, which was reversed by 1 mg/kg (IP) naloxone. Also, hyperalgesia was noted 18 days after the bilateral adrenalectomy of the rats as measured in our laboratory by the hot plate method and as reported by Heybach and Vernikos-Danellis in 1978. These results suggest that the corticosteroid modulation (pituitary-adrenal axis) may have a role in regulating the SIA, and this may implicate the interactions of the corticosteroids with pain-inhibiting systems.
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PMID:Corticosteroid modulation and stress-induced analgesia in rats. 730 Oct 53

The abdominal constriction test was used to explore the effects of cold stress (4 degrees C) of varying duration on the antinociceptive effects of morphine in mice. It was found that after 15 min exposure to cold significant endogenous analgesia was observed, together with a significant potentiation of the antinociceptive effects of morphine. However, after more prolonged exposure to 4 degrees C, the endogenous analgesia was no longer seen and, in addition, the antinociceptive effects of morphine diminished progressively, and after 2 h or longer exposure it was significantly less than control values. It was sown that, in the absence of cold stress, pretreatment with corticosterone, dexamethasone or ACTH reduced the potency of morphine in a manner similar to that seen after 4 h cold stress. It was also shown that the potency of morphine in adrenalectomized mice was not affected by 3 h cold stress. It is concluded that adrenal corticoids, released in response to the stressor effect of exposure to cold, are responsible for the antagonism of the antinociceptive action of morphine seen in mice after extended exposure to cold. It is suggested that the initial potentiation of the antinociceptive potency of morphine is due to the release of endogenous opioids. With more prolonged stress, the stores of these substances may become progressively depleted, possibly as a result of raised corticosteroid levels, so that the component of analgesia contributed by them is steadily reduced and ultimately abolished.
Pain 1980 Aug
PMID:The possibility that a component of morphine-induced analgesia is contributed indirectly via the release of endogenous opioids. 742 38

Teleologically, pain is of paramount importance for survival and induces the organism to cope in an active way with aggressions from a basically hostile environment. While the activation of endogenous analgesic (opioid) systems typically occurs in conditions of surrender (pre-terminal conditions, sustained tortures, etc.), the activation of endogenous anti-analgesic systems triggers mechanisms of active or passive defence (such as camouflage) aimed at survival. The distinctive features of the main anti-analgesic systems (melanocortinergic, cholecystokininergic, thyroliberinergic) and the dramatic results obtained in experimental pre-terminal conditions (hemorrhagic shock, prolonged respiratory arrest) with the administration of their neuropeptide transmitters (ACTH and several ACTH-fragments, including alpha-MSH, CCK peptides and thyrotropin-releasing hormone) are here reviewed. The study of the mechanisms underlying the resuscitating effects of these neuropeptides has led to the discovery of the (often extremely potent) resuscitating effect of other drugs (protoveratrines, nicotine, centrally-acting cholinergic agents, ganglion-stimulating drugs). It is particularly remarkable that in pre-terminal conditions these neuropeptides and drugs have highly impressive effects on cardiocirculatory parameters at doses that are almost or actually inactive under normal conditions, and that their resuscitating effect is obtained without the need for any other supportive treatment and at dose-levels well below toxic ranges. Finally, in hemorrhage-shocked animals, the treatment with anti-analgesic neuropeptides shortly after bleeding considerably extends the time-limit for an effective and definitively curing blood reinfusion. This would be of self-evident importance in clinical practice, because an extremely simple, non-toxic first-aid treatment in the field, shortly after a massive hemorrhage, could resuscitate the patient for a period sufficient to effectively set up the most appropriate in-hospital treatment.
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PMID:The opioid/anti-opioid balance in shock: a new target for therapy in resuscitation. 748 Nov

A 46-year-old woman with rheumatoid arthritis had been on non-steroidal antiinflammatory agents for eighteen years until she developed cushingoid features and hypertension resistant to antihypertensive drugs. She had high plasma cortisol and 24 h urinary 17-hydroxycorticosteroids (17HCS) which were not suppressed by 8 mg dexamethasone per day for two days. The circadian rhythm of plasma cortisol was absent and plasma ACTH concentrations were suppressed before and after intravenous administration of CRH. Abdominal computed tomography demonstrated a tumor (3.0 x 3.0 x 2.3 cm) in the right adrenal gland and a 131I-6 beta-19-nor-methylcholesterol scan revealed marked uptake on the same side. The patient underwent a right adrenalectomy and the diagnosis of a cortisol secreting benign adenoma was histologically confirmed. Blood pressure declined and cushingoid features regressed, but three months after the operation and while the patient was on replacement, she complained of pain on motion, marked tenderness and swelling of fingers, wrists, elbows, knees and foot joints, and had very high rheumatoid factors. Treatment with immunosuppressive drugs and oral and intraarticular administration of glucocorticoids were necessary to relieve the clinical symptoms of rheumatoid arthritis. In summary, we report a patient with rheumatoid arthritis and Cushing's syndrome due to an adrenal adenoma, in whom rheumatoid arthritis was exacerbated after curing the Cushing's syndrome. This suggests that it is imperative to follow the development and/or course of autoimmune diseases after the treatment of Cushing's syndrome.
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PMID:Exacerbation of rheumatoid arthritis after removal of adrenal adenoma in Cushing's syndrome. 762 66

Using the behavioral pharmacological approach, we have studied the influence of ACTH on the analgesia mediated by three types of opioid receptors (mu, delta, kappa). The mechanisms by which ACTH antagonizes opioid analgesia were explored at receptor level and post-receptor second messenger level. The expression of Fos protein induced by ACTH was also observed in rat brain. The main results show that ACTH selectively antagonizes spinal opioid analgesia mediated by mu and delta, but not kappa receptors. The proposed mechanisms of the anti-opioid effect of ACTH are that ACTH can modulate opioid-induced decrease of intracellular cAMP content and the suppression of calcium influx. ACTH has been shown to induce Fos protein expression in selected brain areas including the nuclei involved in pain modulation. These brain areas may serve as sites of action for ACTH to exert its anti-opioid effect.
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PMID:[Adrenocorticotropic hormone (ACTH): antagonistic effect on opioid analgesia in central nervous system of the rat and its possible mechanisms of action]. 765 13

In a prospective study, third trimester plasma levels of BE and ACTH were determined in 58 women who delivered vaginally. Peptide regulation was compared between subjects who used conduction anesthesia at delivery and subjects who did not. Third trimester levels of maternal BE and ACTH were significantly related; however, the relationship was significant only in subjects who did not receive conduction anesthesia (n = 24) at delivery. The normal co-release pattern between BE and ACTH in subjects receiving conduction anesthesia (n = 34) during birth was uncoupled. The use of conduction analgesia during vaginal delivery was significantly related to a disregulation index created to quantify the BE-ACTH release pattern. Uncoupled ACTH and BE patterns may result from modified control of pro-opiomelanocortin (POMC) expression during pregnancy or unique proteolytic processing of POMC, and may alter pain tolerance during delivery.
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PMID:Third trimester POMC disregulation predicts use of anesthesia at vaginal delivery. 778 47

Hypothalamic involvement has been invoked to explain the periodicity of the cluster periods and rhythmicity of the pain attacks in cluster headache. To explore this hypothesis the ovine corticotrophin-releasing headaches sufferers during both cluster period and remission. A group of low back pain patients and healthy subjects comprised the control populations. For the o-CRH test, 7 healthy subjects, 7 low back pain patients, 6 cluster headache patients in remission, and 12 in cluster period were studied. Five healthy subjects, 7 low back pain patients, 6 cluster headache patients in remission, and 9 cluster period were administered the insulin tolerance test. Significantly increased basal cortisol levels were found in cluster headache patients in both illness phases (p < 0.0001), but not in low back pain patients. Significantly reduced cortisol response to the o-CRH test was observed in cluster headache patients in both phases compared to healthy controls (p < 0.02). A blunted ACTH and cortisol response (p < 0.0001 and p < 0.003 respectively) to the insulin tolerance test was present in cluster headache patients in both phases of the illness compared to healthy subjects and low back pain patients. On the contrary, the ACTH surge after insulin induced hypoglycemia was significantly increased in the low back pain patient group (p = 0.02). These results suggest that the altered hypothalamic-pituitary-adrenal axis responsiveness in cluster headache patients is not a consequence of the pain, and point to a central, probably hypothalamic derangement in this pathology.
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PMID:The insulin tolerance test and ovine corticotrophin-releasing-hormone test in episodic cluster headache. II: Comparison with low back pain patients. 782 95


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