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

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

In this review, the emerging functional roles of the brain angiotensin system have been considered. The major effects of Ang II can be classified into three groups, which imply three possible functions: The first, and largest, group is actions associated with the regulation of body fluid volume in response to hypovolemia. These include thirst, blood pressure increase, vasopressin release, sodium appetite and excretion, and ACTH and aldosterone release. This function alone has important implications for the control of blood pressure and the disease of hypertension. Another possible function is a role for angiotensin in the activity of gonadotropic hormone releasing hormones and pituitary hormones during the reproductive cycle and pregnancy. A third group of functions is the synaptic, neurotransmitter interactions of Ang II with catecholamines, serotonin, prostaglandins, and other peptides, not all of which could be reviewed here due to space limitations. This interaction is significant for all functions mentioned and leads to alterations in motivation (thirst, pain), memory (and possibly learning), and motor control. The amount of data available, however, is so limited that to claim angiotensin plays any major role in the latter functions would be premature. Throughout this review, we compared the central and peripheral effects of Ang II. We suggest that normally, a blood-CVO barrier prevents diffusion of peripheral Ang II to brain receptors inside the BBB. Because of this mechanism, the responses to the two routes of administration are distinctly different. When systemic peptide levels are low, Ang II activates only receptors in the CVOs; however, when these levels are high, the peptide diffuses to receptors that are normally activated only by brain Ang II.
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PMID:Functions of angiotensin in the central nervous system. 355 9

In 18 patients scheduled for lower intraabdominal surgery (hysterectomy), changes in thyreotropin (TSH) thyroxine (T4), triiodothyronine (T3) binding of thyroid hormones to plasma proteins (T3-uptake) and glucose in serum were evaluated. In eight patients afferent neurogenic impulses from the surgical area were blocked (Th4-S5) with bupivacaine 0.5% infused continuously into the epidural space from the start of the operation until 6 h postoperatively. All patients received general anaesthesia with thiopentone, pethidine, pancuronium and nitrous-oxide plus oxygen. The patients receiving epidural analgesia had no increase in plasma-TSH, compared to the other group, which had a significant (P less than 0.05) increase peroperatively. The patients receiving epidural analgesia were pain-free and the normal stress-induced increase in plasma-glucose was abolished. Concerning T3 we found a significant decrease in both groups and a steady level of T4- and T3-uptake without significant fluctuations. Thus it can be concluded that the effects of surgical trauma on plasma-TSH concentration are markedly similar to the effects of other anterior pituitary hormones, i.e. HGH, prolactin and ACTH.
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PMID:Per- and postoperative changes in the concentration of serum thyreotropin under general anaesthesia, compared to general anaesthesia with epidural analgesia. 359 Dec 53

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

In order to evaluate the role of endogenous opioids in sustaining analgesia induced by transcutaneous nerve stimulation (TNS), we measured plasma beta-lipotropin (BLPH), beta-endorphin (BEP), ACTH and cortisol changes concomitantly with nociceptive flexion reflex (RIII) threshold after TNS (80 microseconds rectangular waves at 85 Hz) in a group of healthy volunteers (A). The same protocol was carried out in another group of volunteers using placebo stimulation (0.5 Hz) (B). RIII threshold significantly increased 0.5 h after TNS in group A and no changes were recorded in group B. Similarly, both BLPH and BEP plasma levels increased at the end of TNS only in group A. ACTH and cortisol concentrations show only random variations after both high and low frequency TNS. A positive linear correlation was found between the maximum percentage increase of RIII threshold after high frequency TNS and the maximum percentage increase of BLPH plasma levels occurring 20 min beforehand (r = 0.856, P less than 0.001). A less positive correlation was found between RIII and BEP levels (r = 0.574, P less than 0.05). These data indicate that the so-called post-stimulation analgesia could be supported by the enhancement of the endogenous opioid system.
Pain 1984 Jul
PMID:Concomitant increase in nociceptive flexion reflex threshold and plasma opioids following transcutaneous nerve stimulation. 608 74

The endogenous opioids seem likely to be assigned a significant role in the integrated hormonal and metabolic response to exercise. This article reviews the present evidence on exercise and the endogenous opioids, and examines their involvement in a number of widely disparate physiological processes. In considering the role of individual opioid peptides, it is important to remember that many of the tools and techniques now used are still relatively crude. Most studies have demonstrated that serum concentrations of endogenous opioids, in particular beta-endorphin and beta-lipotrophin, increase in response to both acute exercise and training programmes. Elevated serum beta-endorphin concentrations induced by exercise have been linked to several psychological and physiological changes, including mood state changes and 'exercise-induced euphoria', altered pain perception, menstrual disturbances in female athletes, and the stress responses of numerous hormones (growth hormone, ACTH, prolactin, catecholamines and cortisol). Many reports have described a role for the endorphin response as seen during exercise and have used the opioid receptor antagonist, naloxone, to investigate and verify the degree of involvement of the opioids. However, whether the observed increases in peripheral endorphin concentrations are sufficient to cause immediate mood changes, create menstrual cycle dysfunction or alter pain perception is still not resolved. A relatively new implication for the endorphins and associated changes with exercise is in ventilatory regulation. A number of studies have suggested that endogenous opioids depress ventilation and may, therefore, play a role in ventilatory regulation by carbon dioxide, hypoxia and exercise. It may also be possible that during exercise, the perception of fatigue is modulated by an increase of endogenous opioids.
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PMID:Endorphins and exercise. 609 Dec 17

beta-Endorphin31, beta-endorphin1-27, and their alpha-N-acetyl derivatives were specifically separated by ion exchange chromatography from human beta-endorphin-'like' material obtained from extracts and culture media of corticotropic adenomas and extract of plasma from Nelson's syndrome and ectopic ACTH/LPH syndrome. Studies with pituitary-derived materials have shown that human beta-endorphin1-31 was the major form and human beta-endorphin1-27 a minor form. No other peptide was detected. In plasma from the ectopic ACTH-LPH syndrome human beta-endorphin1-31 was the only detected peptide. In 2 such patients with chronic elevation of human beta-endorphin1-31 the pain sensitivity threshold was normal and naloxone induced no modification, suggesting that circulatory human beta-endorphin has no effect on the central nervous system.
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PMID:Molecular forms of beta-endorphin in ACTH/LPH hypersecretion syndromes in man. 609 55

Different levels of exercise (50-200 W) were produced by a bicycle ergometer. In all six subjects the heart rate and blood pressure were increased with increasing work load. Dental pain thresholds tended to increase with increasing work load, too. Plasma ACTH levels were above the normal range during the whole experiment in all subjects, whereas plasma cortisol and prolactin levels were elevated only in one subject. Growth hormone levels had a tendency to elevation at 200 W. There was no correlation between the release of cortisol, prolactin or ACTH and the dental pain threshold elevation. However, there was significant correlation between the release of growth hormone and the dental pain threshold elevation. The results indicate that physical exercise at submaximal work loads is enough to produce a pain threshold elevation in some subjects, with a minor coactivation of stress mechanisms.
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PMID:The influence of exercise on dental pain thresholds and the release of stress hormones. 610 Mar 93

In order to clarify the mechanism of the analgesic effect of ceruletide (CRL), the peptides B-endorphin (BE), ACTH, prolactin (PRL), growth hormone (GH) and substance P were determined in the basal state and following IV CRL administration in 11 patients. CRL, at the dose of 2 ng/kg/min, significantly augmented BE levels in the plasma, and in CSF. Substance P levels were significantly augmented by CRL in the plasma, while ACTH levels were significantly augmented in CSF. GH and PRL levels were not affected by CRL. Placebo had no effect on any of the measured peptides. The effect of CRL on mood and anxiety, known to be affected by opioids, was studied in 14 patients with psychogenic headache. The effect of histamine induced headache on State trait anxiety inventory and on Mood adjective check list was studied before and after administration of placebo or CRL. CRL significantly diminished anxiety when compared to placebo. Elation, surgency and egotism were significantly augmented while skepticism was significantly diminished by CRL. The CRL effect on mood and pain may be mediated by augmented levels of neurohormones both in the plasma and in CSF.
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PMID:Effect of ceruletide on pituitary-hypothalamic peptides and on emotion in man. 617 96

A computerized study of past infectious events and neurological parameters revealed the existence of a history of repeated respiratory-tract infections (RRI) beginning in childhood, in 52% of 251 multiple sclerosis (MS) patients studied. The 251 MS patients were divided into two groups: those without a past history of RRI were designated as "MS type I", and those with a history of infectious problems before the onset of MS as "MS type II". Significant differences in the neurological symptoms, the treatment received and some general parameters were found between the groups, which suggested a correlation between the evolution of MS and the presence or not of RRI in these patients. When compared to the MS type I group, a significantly higher percentage of MS type II patients reported visual problems (P less than or equal to 0.01), paresthesia (P less than or equal to 0.01), loss of sensitivity (P less than or equal to 0.03), pain (P less than or equal to 0.004), motor problems (P less than or equal to 0.016) and sexual dysfunction in males (P less than or equal to 0.02). The mean number of attacks in the first 5 years of the disease was significantly more frequent in MS type II patients, 6.2 compared to 2.9 (P less than or equal to 0.02). A significantly higher percentage of MS type II patients also received oral corticosteroids (P less than or equal to 0.02) or ACTH (P less than or equal to 0.003). Although the age of onset of MS was the same for both groups, MS type II patients were significantly younger than MS type I patients, the mean age being 36 years compared to 41 years (P less than or equal to 0.001). Only 12% of patients in the MS type II group compared to 30% in the MS type I group had the disease for more than 15 years (P less than or equal to 0.001). As is usual with MS, the majority of the patients in both groups were females, 79.3% in the MS type II compared to 63.4% in the MS type I group. These findings suggest that MS patients with a past history of RRI (MS type II) have a different evolution of their disease from MS type I patients and that in general the disease is more severe. The past infectious history of patients would thus appear of putative value, in addition to neurological criteria, in assessing the probable future evolution of the disease.
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PMID:Past infectious events and disease evolution in multiple sclerosis. 619 63


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