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)

We can state that an effective pain relief during labour, like epidural analgesia, is indicated and it prevents or modifies the pain-induced harmful effects on mother and the fetus. Maternal and fetal ACTH or BE response in labour are not altered, but the increase of maternal cortisol secretion is reduced, thus probably suggesting a lesser maternal stress, to which also point the changes of PRL. Epidural analgesia prevents harmful maternal metabolic changes like hyperventilation, hypocapnia, metabolic acidosis and lactic acid accumulation. These beneficial effects are also reflected in a better fetal and neonatal condition. Carbohydrate and fat metabolism, on the contrary, seem not to be significantly changed by epidural analgesia. Epidural analgesia is beneficial also by reducing the pain induced catecholamine release, and by improving the intervillous blood flow, especially in pre-eclamptic parturients.
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PMID:Maternal and fetal effects of epidural analgesia during labour. 299 Jan 22

In order to investigate the involvement of pituitary beta-endorphin in electroacupuncture analgesia (EAA), the effects of hypophysectomy, dexamethasone (Dex) and adrenalectomy on the analgesia and the increase in plasma corticosterone (Cort) and ACTH levels produced by electroacupuncture (EA) were studied in male SD rats. In saline-treated and Dex-treated rats, plasma Cort levels were correlated with plasma ACTH levels. In non-treated rats, the time course of EA-induced increase in pain threshold was similar to that of EA-induced elevation of plasma Cort levels. In the hypophysectomized rats, EAA was significantly reduced and the EA-induced increase in plasma Cort was also abolished. Single administration of a large dose of Dex tended to reduce EAA and significantly reduced the EA-induced increase in plasma Cort and ACTH. Further suppression of pituitary functions by 4 days-treatment with Dex resulted in further reduction of EAA and the EA-induced increase in plasma Cort and ACTH. On the other hand, hind-paw pressure test without EA produced an increase in plasma Cort and ACTH to the same extent as that produced by EA and produced no analgesia. In the adrenalectomized rats, EAA was reduced, and the plasma ACTH level, which was sixteen times higher than that of nonoperated rats, was further elevated 2-fold higher by EA. No correlation between plasma ACTH levels and the increase in pain thresholds was observed in individual rats of the saline-treated and Dex-treated groups. Control pain thresholds were not influenced by hypophysectomy, Dex or adrenalectomy. These results suggest that pituitary beta-endorphin may not be mainly involved in EAA.
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PMID:[The role of the pituitary in the development of electroacupuncture analgesia in rats]. 299 39

The effects of halothane anaesthesia or epidural analgesia on the per- and postoperative change in blood concentrations of ACTH, beta-lipotropin, cortisol, dehydroepiandrosterone, aldosterone, glucose, lactate and free fatty acids were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with halothane and nitrous oxide was found to be associated with a significant increase in plasma ACTH levels and beta-LPH levels. Changes in plasma dehydroepiandrosterone were similar to those in plasma cortisol. The elevation of plasma aldosterone during major surgery could be explained as the effect of an increased renin secretion. However, simultaneous increase in plasma cortisol and plasma aldosterone during surgery reflect an additional effect of adrenocorticotropin upon aldosterone secretion.
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PMID:[Behavior of the hypophyseal-adrenal cortex system in inhalation and conduction anesthesia. A review with comparative study]. 299 12

We investigated the psychoneuroendocrine and emotional correlates of the natural stress situation of human labor. State anxiety, subjective pain, plasma ACTH, peripheral plasma beta-lipotropin (Beta-LPH), beta-endorphin (Beta-EP), and met-enkephalin (Met-Enk) were serially evaluated at six predetermined time points before, and after labor in a sample of 14 women with normal pregnancies. State anxiety and subjective pain showed a progressive increase during labor, with a levelling during the final stage. Plasma Beta-EP and ACTH showed a similar progressive increasing from baseline until the end of labor. Beta-LPH showed no significant modification. Met-Enk remained at nearly baseline values throughout labor, with a marked progressive rise in the postpartum stage. The findings of this study seem to confirm the role of plasma Beta-EP as a stress hormone. Possible relationship between pain and anxiety curves and plasma Beta-EP are discussed in light of psychobiological studies on stress, the opioid system and analgesia. Plasma Met-Enk, according to our findings, should probably not be regarded as a stress hormone. Its rise in the postpartum stage might be as one of the psychoneuroendocrine mechanisms maintaining elevated prolactin levels during lactation.
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PMID:ACTH, beta-endorphin and met-enkephalin: peripheral modifications during the stress of human labor. 299 23

Viral infection of lymphocytes induces the synthesis of interferon (IFN)-alpha and immunoreactive corticotropin (irACTH). We have previously shown the irACTH to be antigenically, structurally, and functionally related (if not identical) to pituitary ACTH. Virus infected lymphocytes also synthesize in endorphin as measured by immunofluorescence. The endorphin-like activity was found to be associated directly with IFN-alpha as well as other, lower molecular weight peptide(s) having no antiviral activity. Crude IFN-alpha at 1000 U/ml exhibited opiate receptor binding activity by inhibiting 47.2% of 3H dihydromorphine (4 X 10(-9) M) binding to mouse brain tissue. Homogeneous HuIFN-alpha (10(8.3) U/mg) also bound to opiate receptors but required 10 times the antiviral activity than crude IFN-alpha for a 50% inhibition of dihydromorphine binding. When injected intracerebrally both crude and homogeneous IFN-alpha induced transient analgesia in mice that was reversible and preventable by the opiate antagonist naloxone. The low molecular weight (less than 10 Kd) ir endorphins purified from the IFN-alpha had no antiviral activity, but may represent the majority of the opiate receptor binding material in the infected lymphocyte culture fluid. These data seem to indicate that the opiate-like side effects of exogenous IFN administration may be due to the IFN-alpha molecule binding to opiate receptors and also may be due to the associated low molecular weight endorphin-like moieties synthesized by lymphocytes.
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PMID:Opiate receptor mediated effects of IFN-alpha and lymphocyte derived endorphin-like peptides. 300 57

In order to demonstrate pharmacokinetic and pharmacodynamic interactions between fentanyl and buprenorphine, 3 groups of patients (n = 30) were compared, receiving either fentanyl (0.005 mg/kg b.w.) or buprenorphine (0.01 mg/kg b.w.) or both opioids as analgesic during surgery for disc protrusion. For a period of 4 h haemodynamic parameters were monitored and blood samples were taken for determination of the following concentrations: ADH, ACTH, cortisol, glucose, unbound glycerol, fentanyl and buprenorphine. Blood gas analyses were performed up to 2 h postoperatively. Although in all groups haemodynamic parameters were constant, there was an increase in factors related to operative stress (cortisol, glucose, unbound glycerol, postoperative acidosis) after the combination of both opioids, while postoperative ventilatory parameters in this group were not improved by the partial agonist buprenorphine. Plasma levels were not affected by combined application, except for a slight elevation of buprenorphine concentrations during additional use of fentanyl. Buprenorphine, at least in higher dosages, seems to antagonize analgesia induced by fentanyl, although respiratory depression is even more pronounced. It may be assumed, that with partial agonists the relation of agonistic and antagonistic activity may be different, depending on the dosage used and on the respective pharmacologic effect observed during investigation.
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PMID:[Intra- and postoperative interactions between the 2 opioids fentanyl and buprenorphine]. 301 44

The effect of prenatal ethanol exposure on pituitary-adrenal function in adult offspring was assessed by measuring corticosterone (CS) levels in plasma following exposure to two forms of footshock stress, intermittent and continuous, and after administration of 20 mg/kg of morphine. The footshock experiments were conducted at two time points in the circadian pituitary-adrenal cycle. Prenatally ethanol-exposed (E) rats had higher levels of CS than pair-fed and normal controls following intermittent footshock when tested at the crest of the CS circadian rhythm. However, this difference was not present when intermittent footshock was presented at the trough of the circadian cycle. At either time of day, there were no differences among the prenatal treatment groups in the basal condition or following continuous footshock. In addition, E rats had significantly higher levels of plasma CS than controls following morphine. Plasma adrenocorticotropin (ACTH) levels were measured after intermittent footshock at the crest of the circadian rhythm and were significantly higher in E rats than in controls. These results extend our previous reports of enhanced activation of the hypothalamo-pituitary-adrenal axis in response to other stressors as well as to ethanol in adult rats exposed to ethanol in utero. They also confirm that E rats are differentially hyperresponsive only to intermittent footshock stress, not to continuous footshock, as we had found to be the case when the analgesia induced by these two stressors was the dependent measure.
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PMID:Pituitary-adrenal responses to morphine and footshock stress are enhanced following prenatal alcohol exposure. 301 74

Endogenous opioid peptides (EOP) participate in a variety of physiological and pharmacological responses that can be recognized by: increased concentrations of EOP in the cerebrospinal fluid; a combination of euphoria and analgesia; and suppression of the responses by specific opiate antagonists. Application of these responses is exemplified in acupuncture, in self-stimulation via hypothalamic electrodes, and in food and fluid consumption. For example, intake of sweet solutions exerts a biphasic effect: in the beginning pain threshold is elevated, but later on tolerance to morphine-induced analgesia develops. A supply of 2% NaCl also stimulates fluid intake as well as raising the pain threshold. Stress-induced analgesia is due to coupled release of ACTH and beta-endorphin from the pituitary. In man, large variations in pain sensitivity may be related to the level of intrinsic EOP.
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PMID:The role of endogenous opioid peptides in physiological and pharmacological reward responses--a survey of present-day knowledge. 303 50

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

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


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