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

We have investigated plasma beta-endorphin (beta-E), ACTH, and cortisol in two cases of congenital indifference to pain (CIP), a rare syndrome characterized by unresponsiveness to painful stimuli. As the two patients had frequent skin infections, we also studied lymphocyte response to mitogens in the absence or presence of beta-E. In addition, we explored a series of lymphocyte membrane antigens related to different aspects of the immune response, such as CD3+, CD4+, CD8+, B, NK Leu 7, Leu 9, and Leu 19, anti-interleukin-2 receptor (anti-TAC). Plasma beta-E levels in the two patients were significantly higher than in controls, whereas plasma ACTH and cortisol levels were normal. Lymphocyte response to the mitogen phytohemagglutinin was normal. The expression of Leu 7, Leu 9, and Leu 19, three antigens related to natural killer cells, was decreased by about 50%. The results indicate that in the two cases of CIP studied, high plasma beta-E levels are associated with a reduction in the expression of natural killer cells. This suggests that the two phenomena are specifically related to each other. These data represent further evidence of the possible pathophysiological relevance of the neuroendocrine-immune feedback.
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PMID:Plasma beta-endorphin levels and natural-killer cells in two cases of congenital indifference to pain. 137 38

Exercise-induced increases in the peripheral beta-endorphin concentration are mainly associated both with changes in pain perception and mood state and are possibly of importance in substrate metabolism. A more precise understanding of opioid function during exercise can be achieved by investigating the changes in beta-endorphin concentrations dependent upon intensity and duration of physical exercise and in comparison to other stress hormones. Published studies reveal that incremental graded and short term anaerobic exercise lead to an increase in beta-endorphin levels, the extent correlating with the lactate concentration. During incremental graded exercise beta-endorphin levels increase when the anaerobic threshold has been exceeded or at the point of an overproportionate increase in lactate. In endurance exercise performed at a steady-state between lactate production and elimination, blood beta-endorphin levels do not increase until exercise duration exceeds approximately 1 hour, with the increase being exponential thereafter. beta-Endorphin and ACTH are secreted simultaneously during exercise, followed by a delayed release of cortisol. It is not yet clear whether a relationship exists between the catecholamines and beta-endorphin. These results support a possible role of beta-endorphin in changes of mood state and pain perception during endurance sports. In predominantly anaerobic exercise the behaviour of beta-endorphin depends on the degree of metabolic demand, suggesting an influence of endogenous opioids on anaerobic capacity or acidosis tolerance. Further investigations are necessary to determine the role of beta-endorphin in exercise-mediated physiological and psychological events.
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PMID:Changes in beta-endorphin levels in response to aerobic and anaerobic exercise. 155 53

A limited number of experiments have shown that treatment of rheumatoid arthritis by means of cooling the entire body in cryogenic chamber reduces the pain in joints affected by inflammatory process and increases their mobility. The aim of the present thesis was to try explain the mechanisms responsible for the observed improvement of the patients' condition, and an investigation of the treatment's effect on selected hemodynamic indices. Tests were carried out on 63 patients with rheumatoid arthritis mainly in the 3rd and 4th stage of illness, all of whom had been treated for 14 days, once daily, by cooling the body for two-minute periods in cryogenic chamber with temperatures ranging from -110 degrees C to -160 degrees C, followed by kinesitherapy. It was demonstrated that after a single session in the cryogenic chamber, after 7 and 14 days the level of ACTH, cortisol and beta-endorphins in blood serum rises. The level of TSH, T4, T3, GH and 6-keto-PGF1 alpha+, however, remains unchanged. The cryogenic chamber treatment does not affect the heart rate, arterial blood pressure nor the value of the left ventricle fractional shortening index and its ejection, neither does it cause of arrhythmias and ischemic changes of the heart.
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PMID:[Hormonal and hemodynamic changes caused by whole body cooling in patients with rheumatoid arthritis]. 164 62

Analgesia (NAA) caused by nonacupuncture point (abdominal muscle) stimulation after lesioning the analgesia inhibitory system (AIS) or treating the subject with proglumide was abolished by hypophysectomy or adrenalectomy. The final sector of the NAA afferent pathway from the nonacupuncture point to the pituitary gland and the initial sector of the descending pain inhibitory system were found in the anterior and posterior arcuate nucleus (A-HARN and P-HARN), respectively. Analgesia caused by ACTH microinjected into the P-HARN disappeared after denervation of the A-HARN, but that caused by dopamine did not. Firing rates of P-HARN neurons were increased by nonacupuncture point simulation (NAPS) after lesion of the AIS or treatment with proglumide. The NAPS responsive neurons also responded to ultramicroinjected dopamine, but not to ultramicroinjected ACTH. Both NAA and NAPS responsive neuron activity that were abolished by hypophysectomy were restored by concurrent application of NAPS and intraperitoneal ACTH. Reduction of sodium ions due to adrenalectomy was found to abolish NAA. It was concluded that NAA production involves dopaminergic transmission in the HARN and ACTH acting presynaptically on this transmission.
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PMID:Analgesia produced by pituitary ACTH and dopaminergic transmission in the arcuate. 165 17

Pigs' responses to physical restraint were examined in order to detect a stress-induced increase in endogenous opioid activity. Tail-flick latencies in response to a source of thermal energy were used to assess the sensitivity of pigs to pain. Restraining pigs for 15 min with a nose snare resulted in a temporary increase in tail-flick latencies that was apparent after 5 min, absent after 30 min and was blocked by naloxone. Tail-flick latencies were unaffected by IV ACTH injections and were not related to plasma cortisol concentrations. Naloxone increased the pigs' vocalization during the restraint and prolonged the elevation of plasma cortisol levels that followed the restraint. The cortisol response to naloxone was larger than when the animals were not restrained. The results indicate a transient, opioid-based hypoalgesia following restraint stress that is not a result of ACTH or cortisol secretion. Endogenous opioids inhibit the pigs' behavioral and pituitary-adrenocortical responses to the restraint stress.
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PMID:Stress-induced hypoalgesia and opioid inhibition of pigs' responses to restraint. 166 15

Stress can be defined as a "reaction by living beings to any relevant impairment". The effect of anaesthesia on endocrine function is closely related to the actual stress concept based on the works by Cannon and Selye. Cannon described the role of catecholamines in stress and characterised the fight-flight reaction. Selye emphasised the role of the adrenocortical reaction defining the "general adaptation syndrome", which evolves in three stages ("alarm reaction", "stage of resistance", "stage of exhaustion"). Later, Henry postulated the dual stress concept. The sympathetic-adrenomedullary system is activated during the fight-flight reaction, thus representing an active role of the organism. The pituitary-adrenocortical system is activated during loss of control, submission and depression, especially in a social context. Main valid parameters of this endocrine stress response are adrenaline, noradrenaline, ADH, ACTH and cortisol. In the perioperative period, both pathways are "stressed". The most important factors are patient, operation, and anaesthesia. Anaesthesia can influence the stress response by afferent blockade (local anaesthesia), central modulation (general anaesthesia) or peripheral interactions with the endocrine system (etomidate). Up to now, a total peripheral blockade of the nociceptive system is impossible, due to surgical technique (destruction of nerve fibres) and release of mediator substances. With regard to reduction of endocrine stress response, inhalation anaesthesia with volatile anaesthetics and nitrous oxide may be less effective than neuroleptic, spinal or epidural anaesthesia. Immediately after extubation, rapid increases of endocrine parameters are observed. In addition to central modulation of pain and stress, both halothane and enflurane inhibit catecholamine release from the adrenal medulla. Neuroleptic anaesthesia and total intravenous anaesthesia are very potent and sufficient to control the increases in endocrine parameters even during major surgery, due to their central effects. Spinal and epidural anaesthesia alone as well as in combination with general anaesthesia can reduce the endocrine stress response more than necessary. This is due to the sympathetic blockade, combined with an afferent blockade of central cord fibers which modulate the pituitary-adrenocortical system. Only few data are available concerning the stress response during infiltration anaesthesia or nerve block, but additional sedation seems to be beneficial. Peripheral interactions with the endocrine system like blockade of the adrenal cortex by etomidate is dangerous and has caused a high mortality in intensive-care patients if the substance was admitted for a longer period. Assessment of endocrine stress response in anaesthesia and surgery is controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The endocrine stress reaction in anesthesia and surgery--origin and significance]. 175 50

Twenty-eight patients undergoing upper abdominal operations (mainly selective proximal vagotomy [SPV]) were referred for assessment of the hormonal metabolic reaction (adrenocorticotropic hormone [ACTH], arginine vasopressin [AVP], cortisol, and glucose), the postoperative pain reaction, and respiration according to the method of anesthesia (group 1: neuroleptanesthesia [NLA], group 2: NLA in combination with epidural opiate analgesia, group 3: NLA in combination with local anesthesia). To alleviate postoperative pain piritramide was systematically administered in group 1, whereas in groups 2 and 3 a thoracic epidural catheter was injected with morphine or bupivacaine. Postoperative analgesia was better in patients with epidural administration than in those with systemic application. On the 1st and 2nd postoperative days the vital capacity was statistically significantly higher by 10%-15% in groups 2 and 3 than in group 1. As expected, the neurohormonal and metabolic stress response was highest in all patients in the intraoperative and immediate postoperative phases: ACTH, AVP, and glucose levels were in most cases significantly higher compared with the initial values. However, cortisol levels decreased intraoperatively, probably as a result of the generally used induction agent etomidate. Comparison of the three methods of anesthesia revealed that all mean hormone levels analyzed in group 2 patients were lower both intraoperatively and 2 h postoperatively, which implies that epidurally administered morphine reduces the stress reaction, probably indirectly through additional selective alleviation of pain at the spinal cord level. The various differences in hormonal reactions of patients in groups 1 and 3 gave no clear evidence, however, of possible mitigation of the stress reaction by epidural local anesthetics in upper abdominal operations.
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PMID:[The effect of combination epidural anesthesia techniques in upper abdominal surgery on the stress reaction, pain control and respiratory mechanics]. 175 31

The immunocytochemical distribution of CLIP (corticotropin-like intermediate lobe peptide) or ACTH(18-39), a small biologically active peptide, was examined in the human brain, using a monoclonal antibody against this peptide. Groups of CLIP-immunoreactive cell bodies, small to medium size and bipolar or triangular in shape, were found in the basal hypothalamus extending from the retrochiasmatic region to the premammillary nuclei area. Immunoreactive fibers with varicosities, terminals and "pipe shape" structures, were distributed within the hypothalamus, limbic structures, the brainstem and spinal cord nuclei, forming a particularly rich network in the hypothalamus, the preoptic area, the septal region, the amygdala and the upper brainstem periaqueductal gray matter. The above neuroanatomical observations confirm and extend previous findings in animals, strengthening even more the possibility that this peptide may be involved in numerous behavioral, autonomic and physiological functions such as regulation of sleep-waking cycle, pain control and respiratory and cardiovascular regulation.
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PMID:Immunohistochemical distribution of corticotropin-like intermediate lobe peptide (CLIP) immunoreactivity in the human brain. 184 84

In experiments on rats the influence was studied of tropic hormones of adenohypophysis--somatotropin, thyrotropin and adrenocorticotropin (STH, ThTN and ACTH respectively) on the elaboration and extinction of conditioned reaction of active avoidance (CRAA) in Y-maze and behaviour in the open field under microinjections of hormones into the brain lateral ventricle (0.001-0.002 ME). It has been shown that all studied hormones improve animals learning at negative pain reinforcement; ThTH and ACTH retard it in contrast to STH, which accelerates the extinction of the elaborated CRAA; tropic hormones exert differentiated influence on rats behaviour in the open field. No distinct correlation was found between behavioural manifestation and the level of catecholamines in the rats hypothalamus.
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PMID:[The action of tropic adenohypophyseal hormones when administered intraventricularly on rat behavioral reactions]. 196 59

Neuroendocrine and autonomic responses were assessed in chloralose-anesthetized cats after chemical stimulation of medial brain-stem regions, including those that influence nociceptive input to the medullary or spinal dorsal horn. Microinjections of L-glutamate (0.5 M, 160 nl) were directed at the following rostral and caudal raphe nuclei: the periaqueductal gray (PAG), the dorsal raphe nucleus (DR), the raphe magnus (RM), and the raphe obscurus/raphe pallidus (Ro/Rpa). Activation of DR neurons evoked a significant increase in the adrenal secretion of epinephrine (+2.6 +/- 1.1 ng/min, P less than 0.01) that returned towards prestimulus values by 6 min, whereas microinjections into other raphe nuclei had no consistent effect. Activation of Ro/Rpa neurons evoked an increase in the plasma concentration of adrenocorticotropin (ACTH, +47.9 +/- 12.3 pg/ml, P less than 0.01), whereas microinjections into other raphe nuclei did not affect ACTH. Arterial pressure increased significantly after activation of PAG (+7.5 +/- 2.1 mm Hg, P less than 0.01) or of DR (+4.8 +/- 2.0 mm Hg, P less than 0.05) neurons, whereas heart rate increased significantly (P less than 0.05) after stimulation of cells within the Ro/Rpa. Glutamate microinjections within the RM, a raphe nucleus that exerts a significant descending influence on nociceptive input to the medullary and to the spinal dorsal horns, had no consistent effect on any measured variable. No evidence was seen to suggest that chemical activation of neurons within raphe nuclei inhibited the adrenal secretion of catecholamines or inhibited the release of ACTH. The results indicated that glutamate activation of neurons within different raphe nuclei evoked non-uniform effects on neuroendocrine and autonomic function. Further, these data suggested that the neural substrate underlying the control of the adrenal secretion of catecholamines and of the release of ACTH in response to activation of raphe neurons is likely distinct from that which contributes to the descending influence on nociceptive input to the medullary and spinal dorsal horn.
Pain 1990 Jul
PMID:Comparison of the influence of rostral and caudal raphe neurons on the adrenal secretion of catecholamines and on the release of adrenocorticotropin in the cat. 197 77


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