Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. We examined the effect of ischaemic pain and sustained isometric muscle contraction on plasma immunoreactive gamma-lipotropin (gamma LPH), beta-endorphin/beta-lipotropin (beta END/beta LPH) and corticotropin (ACTH), which are all synthesized from a common precursor (pro-opiocortin), and plasma cortisol in 10 normal subjects. 2. Experimental pain was produced by inflation to 250 mmHg of a sphygmomanometer cuff, placed above the elbow of the 'dominant' arm, after which the subject squeezed a hand dynamometer, loaded to 12 kg, 20 times at 2 s intervals. Blood was drawn before, after 5 and 10 min of pain, and 30 min after release of the cuff. In a control session, the subjects were asked to squeeze the handgrip alone for 5 min at 30% of their maximum strength, a procedure which elevates the blood pressure without causing pain. 3. One subject had unexplained high (30--71 pmol/l) baseline peptide concentrations. Baseline values for the nine other subjects were: ACTH, 7.3 +/- 1.9 pmol/l (mean +/- SEM); gamma LPH, 18.6 +/- 1.0 pmol/l; beta END/beta LPH, 10.0 +/- 1.1 pmol/l; cortisol, 599 +/- 55 nmol/l. Neither procedure significantly increased the plasma concentration of ACTH or any other peptide, whereas plasma cortisol was significantly increased at both 5 min and 10 min. Plasma ACTH was positively correlated with plasma gamma LPH (r = 0.701; P less than 0.001), beta END/beta LPH (r = 0.970; P less than 0.001) and plasma cortisol (r = 0.758; P less than 0.05). 4. The present study demonstrates that, in normal man, plasma endorphins do not change with experimental ischaemic pain. The rise in plasma cortisol without concomitant rise in ACTH is not explained, but suggests the action of some other agent at the level of the adrenal cortex.
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PMID:The response of plasma immunoreactive adrenocorticotropin, beta-endorphin/beta-lipotropin, gamma-lipotropin and cortisol to experimentally induced pain in normal subjects. 628 7

The effect of ceruletide (CRL), a synthetic decapeptide analogue of cholecystokinin, on rest pain and arterial blood flow was evaluated in 8 patients with advanced, occlusive atherosclerosis of the lower extremities. CRL 1, 2, or 4 ng kg-1 or placebo were infused intravenously in random order, and in a double-blind fashion. Pain relief, assessed by a scoring system, was significantly better (p less than 0.01) following the 2 and 4 ng kg-1 doses of CRL (2.71 and 2.66, respectively) than following placebo (0.75). Arterial blood flow was not affected by either CRL in any dose or by placebo. Pretreatment with naloxone, a pure opioid antagonist, abolished the analgesic effect of CRL. Following the 2 ng dose of CRL, beta-endorphin levels were significantly elevated from a basal value of 125 +/- 15 pg/ml to 191 +/- 35 pg/ml 5 h after CRL administration (p less than 0.05). Circulating levels of ACTH, prolactin and GH were not affected by CRL. It is concluded that CRL was effective in relieving ischaemic rest pain, and that the mechanism was related to the release of endogenous opioids.
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PMID:Effect of ceruletide on rest pain in patients with arterial insufficiency of the lower extremity. 629 Feb 28

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.
Pain 1982 Aug
PMID:Dental analgesia produced by non-painful low-frequency stimulation is not influenced by stress or reversed by naloxone. 629 Sep 63

Beta-endorphin appears to play a definite role in the biologic response to stress and in the endogenous mechanism of pain perception. Opiates exogenously administered during surgery decrease or even suppress the activation of "stress hormones" such as ACTH and cortisol. In the present study, the authors tried to assess the effects of fentanyl administration on plasma beta-endorphin immunoreactivity PBE(ir) during surgical stress. In one group of nine patients, a standard enflurane-based general anesthetic technique without opiates was used for a staging laparotomy. A second group of ten patients undergoing the same type of surgery received fentanyl (10-20 micrograms/kg) as the primary anesthetic drug. In both groups, multiple blood samples were collected prior to, during, and after surgery, following the same time protocol. PBE(ir), plasma cortisol and, in five patients, plasma ACTH were determined by radioimmunoassay. There was no significant change in PBE(ir) in either group after anesthetic induction. Unlike the enflurane group, the fentanyl group did not demonstrate any significant increase from baseline in PBE(ir) during surgery. There was a significant group difference between enflurane and fentanyl in PBE(ir) levels for both "early" and "late" surgery values, but not for the "awake" values (recovery period) where both groups had elevated PBE(ir) levels. Plasma cortisol and plasma ACTH changes followed a trend similar to those of PBE(ir). The suppression of both cortisol and PBE(ir) responses during surgery after administration of fentanyl provides further evidence for the involvement of the endorphin system in the stress response and for its physiologic association with the hypothalamo pituitary axis.
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PMID:Effects of fentanyl on the response of plasma beta-endorphin immunoreactivity to surgery. 629 44

Ischemic pain was produced by a blood pressure cuff placed to the arm of healthy human subjects for 15 min which produced a mean pain score of 59% (visual analogue scale). Ischemia induced a significant dental pain threshold elevation (mean 67%) and 2 mg of naloxone did not reduce it. Thermal sensitivity of the upper lip had a tendency to reduction during ischemia and 2 mg of naloxone reduced this effect. Tactile thresholds in the forehead or in the contralateral arm were not markedly elevated. Neither ACTH nor prolactin level in the plasma was related to the dental pain threshold elevation during ischemia. The findings of the present study suggest that ischemic pain nonsegmentally produces a predominant inhibition of responses to thin afferents. Endogenous opioids may markedly contribute to the reduction of thermal sensitivity induced by ischemia, but their contribution to dental pain threshold elevations seems to be less important. Stress or other adenohypophyseal mechanisms involving the release of ACTH or prolactin do not explain the effects of ischemia found in the present study.
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PMID:Ischemic pain nonsegmentally produces a predominant reduction of pain and thermal sensitivity in man: a selective role for endogenous opioids. 629 48

Epidural micro-injection of morphine hydrochloride is very useful for the postoperative analgesic method. In this study, we investigated the relationship between appearance of amelioration of pain and the plasma prolactin (PRL), growth hormone (GH) and ACTH levels following epidural morphine. The plasma PRL levels significantly elevated with surgical stress. Following epidural morphine, the plasma PRL levels significantly decreased in the effective cases, and significantly increased in the ineffective cases. Following epidural morphine, the plasma ACTH levels significantly decreased in the effective cases, and insignificantly increased in the ineffective cases. The duration to onset of amelioration of pain was prolonged with intravenous injections of metoclopramide (MCP) before epidural morphine. We concluded that patterns of PRL and ACTH releases following epidural morphine were correspondent with the analgesic effect, and that appearance of amelioration of pain following epidural morphine may depend upon the dopaminergic mechanism.
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PMID:[Studies on changes of the plasma prolactin, growth hormone and ACTH levels following surgical stress and epidural micro-injections of morphine hydrochloride as a postoperative analgesic method]. 629 92

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

The immunocytochemical distribution of ACTH1-39 (adrenocorticotropin hormone), a member of the opiocortin family of peptides, was examined in the brainstem of the rat. Immunoreactive ACTH fibers were localized in many serotonin-containing raphe nuclei and in the norepinephrine- and dopamine-containing regions throughout the brainstem. Brainstem areas involved in pain mediation contained immunoreactive ACTH fibers as well as several cranial nerve nuclei and nuclei associated with cardiovascular and respiratory functions.
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PMID:Immunocytochemical localization of ACTH1-39 in the brainstem of the rat. 631 27

We report a 59 year old woman who presented with double vision, nuchal pain and mild dementia. On neurological examination she demonstrated third, sixth and seventh nerve palsies and ataxia. Following intravenous ACTH and oral prednisone therapy she showed a remarkable recovery which left her with only a left facial weakness. She remained well for two years. She then developed bulbar palsy and profound dementia. Pathological examination revealed progressive supranuclear palsy (PSP). This patient demonstrated a greater variability in the course of PSP than has previously been recognized.
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PMID:An atypical case of progressive supranuclear palsy. 632 50

Common migraine (CM) is an evolutive disease characterized by a progressive increase in the number of attacks and a consequent reduction in the free periods, eventually reaching a state of continuous migraine with interparoxysmal headache (MIH). To evaluate the role of central pro-opiocortin-related peptides in the pathogenesis of the disease, cerebrospinal fluid (CSF) levels of beta-lipotropin (beta-LPH), beta-endorphin (beta-EP) and ACTH were measured in two groups of migraine sufferers with increasing severity of the disease (CM and MIH), and in healthy controls. ACTH values were similar in the 3 groups, while beta-LPH levels were significantly lower (P less than 0.005) in patients affected by MIH (10.4 +/- 8.6 fmol/ml) than in patients with CM (35.7 +/- 8.3) and in controls (32.9 +/- 15.33). beta-EP levels were closely correlated with the severity of the disease: they decreased significantly from those found in healthy controls (86.1 +/- 37 fmol/ml) to those of CM sufferers (38.5 +/- 3.5; P less than 0.005) and showed a further significant fall (P less than 0.01) to the lowest levels which were found in MIH patients (14.8 +/- 9.8). These data showing that the progressive evolution of migraine is concomitant with a progressive impairment in the CSF levels of beta-EP, sustain the concept that non-organic central pain is related to a reduced activity of the neurons responsible for the CSF content of beta-EP.
Pain 1984 Feb
PMID:Progressive impairment of CSF beta-EP levels in migraine sufferers. 632 56


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