Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidural analgesia inhibits several metabolic effects of trauma. Some of these effects are generated by the endogenous fever mediator interleukin-1. Postoperative fever was therefore studied in 52 patients, 25 of whom had had epidural analgesia and 27 general anaesthesia. Transvesical prostatectomy was used as standard surgical trauma. Most of the patients had postoperative temperature rise exceeding 0.5 degree C, but the rise was not influenced by epidural analgesia. These data suggest that the release of endogenous fever mediator is not under control of afferent pathways from the region of trauma. The findings are also consistent with regulation of interleukin-1 release which is independent of adrenal stimulation, cyclic AMP or beta-endorphin, as epidural analgesia prevents postoperative increase of these hormones.
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PMID:Influence of neural pathways on the pyrexial response to surgical trauma. 387 48

The adrenocortical response to a short tetracosactrin (Synacthen) test was studied in 11 patients receiving either etomidate infusion or thiopentone infusion used to maintain anaesthesia for abdominal hysterectomy. Pethidine was used as the narcotic component. The results showed that etomidate infusion (median 28.5 ug/kg/min) completely blocked the adrenocortical response to corticotropin stimulation for at least 24 h after surgery. No suppression was found in patients receiving thiopentone infusion. It is concluded that etomidate cannot be recommended for routine induction and maintenance of anaesthesia.
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PMID:Etomidate infusion and adrenocortical function. A study in elective surgery. 403 33

Anterior hypothalamic implantations of crystalline atropine markedly inhibit the adrenocortical responses evoked by surgical stress, ether anesthesia, or intravenolus injection of arginine vasopressin. Similar implants in nearby regions of the brain or sham implantations in the same region were ineffective. The data suggest that the hypothalamic control of pituitary corticotropin may have a cholinergic component.
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PMID:Corticotropin release: inhibition by intrahypothalamic implantation of atropine. 429 46

Techniques are described in detail for a radioimmunoassay of plasma adrenocorticotropin (ACTH) that is capable of detecting hormone in unextracted normal human plasma at 1:5 dilution under the conditions described. The sensitivity of the assay is at the level of 1 mumug/ml (equivalent to 0.014 mU/100 ml). In normal subjects ACTH concentrations averaged 22 mumug/ml (equivalent to 0.308 mU/100 ml) plasma at 8-10 a.m. In a smaller group the concentrations averaged 9.6 mumug/ml (equivalent to 0.134 mU/100 ml) at 10-11 p.m. Although a circadian rhythm in normal subjects was not always well marked throughout the daytime hours, plasma ACTH usually fell to its lowest value in the late evening. In hospital patients who were not acutely ill, concentrations were infrequently above 100 mumug/ml in the morning and usually fell to significantly lower levels in the late evening. Severely ill hospital patients occasionally exhibited a.m. concentrations above 200 mumug/ml. In a group of subjects showing frequent spiking of plasma 17-OHCS concentrations throughout the day parallel spiking of plasma ACTH as well was generally observed.Metyrapone produced marked increases in plasma ACTH within 24 hr in all cases and generally within 3-6 hr except when started late in the day. Dexamethasone brought about a persistent reduction in plasma ACTH in a patient under continued treatment with metyrapone.Hypoglycemia, electroshock, surgery under general anesthesia, histalog and vasopressin administration were usually followed by significant increases in plasma ACTH concentration. Prior administration of dexamethasone blocked the response to hypoglycemia. Marked elevations in plasma ACTH were observed in patients with adrenal insufficiency off steroid therapy, in Cushing's disease after adrenalectomy even in the presence of persistent hypercortisolemia, and in some untreated patients with Cushing's disease. Umbilical cord blood contained higher plasma ACTH concentrations than maternal blood at delivery in seven of eight cases. After suppression of ACTH secretion by dexamethasone or cortisol. ACTH disappeared from plasma with half-times ranging from 22 min to 30 min in three cases studied.
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PMID:Radioimmunoassay of ACTH in plasma. 430 80

Handled female Wistar rats were exposed to one of the following stress stimuli: restraint, electric foot shocks, passive avoidance situation, ether, or nembutal anesthesia followed by ip formalin or laparotomy. Trunk blood was collected 2-4 min after initiation of the stress stimulus for the determination of immunoreactive beta-endorphin (beta-ENDi), ACTH (ACTHi), and alpha-MSH (alpha-MSHi). All stressors evoked a rapid increase of circulating beta-ENDi to 0.75-2.10 ng/ml. All except passive avoidance situation also induced a rapid increase of plasma ACTHi to 0.45-0.70 ng/ml, whereas plasma alpha-MSHi increased after ether and restraint to 0.18-0.40 ng/ml but was not affected by formalin stress. To study the involvement of a beta-adrenoceptor mechanism in stress-induced peptide secretion, rats were treated with D-propranolol or L-propranolol 40 min before stress exposure. Propranolol did not prevent the increase of plasma ACTHi to any of the stressors studied. L-Propranolol but not its inactive D-isomer reduced (restraint, passive avoidance) or abolished (electric foot shocks) the increase in plasma beta-ENDi but did not affect the beta-ENDi response to other stressors (ether, formalin, laparotomy). Similarly, L-propranolol attenuated the alpha-MSHi response to restraint but not to ether stress. To discriminate between corticotroph or melanotroph origin of beta-ENDi released during stress, rats were treated with dexamethasone or were subjected to neurointermediate lobectomy (4 weeks). Neurointermediate lobectomy did not affect basal or stress-induced plasma ACTHi but resulted in undetectable alpha-MSHi levels. It largely prevented the beta-ENDi response to restraint stress (propranolol sensitive) but had little effect on the beta-ENDi response to formalin stress (propranolol insensitive). Conversely, dexamethasone prevented stress-induced ACTHi response without affecting plasma alpha-MSHi. The beta-ENDi response to restraint stress (propranolol sensitive) was not changed but the response to formalin stress (propranolol insensitive) was largely prevented by dexamethasone. These results show that the intermediate lobe is the main source of beta-ENDi secreted during exposure to stressors with a high emotional impact. Since intermediate lobe peptide secretion induced by such stimuli can be prevented by beta-adrenoceptor blockade, we speculate that stress-induced discharge of catecholamines, possibly from the adrenal medulla, is the trigger signal for peptide secretion from the melanotrophs during this type of stress.
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PMID:The beta-adrenoceptor-blocking drug propranolol prevents secretion of immunoreactive beta-endorphin and alpha-melanocyte-stimulating hormone in response to certain stress stimuli. 608 82

Thirty-three patients with major depressive illness were treated with electroconvulsive therapy (ECT) and plasma adrenocorticotropin (ACTH), and cortisol levels were measured 30 min before and 1, 5, 15, 30 and 60 min after ECT. There was an immediate release of ACTH with a maximum after 5 min. The maximum cortisol plasma levels were measured 30 min after ECT. No change in ACTH and cortisol concentrations was seen in control experiments when the patients received only anaesthesia. ACTH release was seen in patients treated with ECT in the morning and in the evening. In 15 patients the levels were studied at the first and sixth (last) ECT. ACTH and cortisol levels were significantly higher after the first ECT as compared with the sixth. This alteration in ACTH release might reflect ECT-induced changes in the central monoaminergic transmission with stimulation of beta-adrenergic pathways leading to inhibition of ACTH-release.
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PMID:Plasma pattern of adrenocorticotropin and cortisol during electroconvulsive therapy in patients with major depressive illness. 609 35

Beta-Endorphin was measured by radioimmunoassay in peripheral plasma of nonpregnant women (58 +/- 2.4 pg/ml, n = 17, mean +/- SE), during the first trimester (47 +/- 2.4 pg/ml, n = 11), the second trimester (33 +/- 1.9, n = 11), and the third trimester (49 +/- 2.7 pg/ml, n = 10) of pregnancy, during early (202 +/- 32 pg/ml, n = 12) and advanced labor (389 +/- 78 pg/ml, n = 10), and 30 to 60 minutes post partum (177 +/- 22 pg/ml, n = 12). Mean plasma levels of beta-endorphin were significantly lower in each trimester of gestation than the levels in nonpregnant control subjects. During labor and the early postpartum period, maternal plasma levels of beta-endorphin were significantly elevated. Furthermore, peripheral plasma levels of beta-endorphin during labor fell from 189 +/- 31 to 97.6 +/- 12 pg/ml (n = 13, p = 0.015) in response to epidural anesthesia, as compared to peripheral plasma concentrations of beta-endorphin of 223 +/- 71 and 193 +/- 47 pg/ml prior to and after injection of saline solution into epidural catheters, respectively, in 10 control subjects. Mean plasma levels of beta-endorphin in patients immediately prior to elective repeat cesarean section who were not in labor (151 +/- 23 pg/ml, n = 15) were significantly higher (p less than 0.005) than the levels in third-trimester control subjects. These data indicate that the pain associated with labor and the psychological stress of anticipating an operation are potent stimuli for the pituitary release of beta-endorphin.
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PMID:Plasma beta-endorphin concentrations prior to and during pregnancy, in labor, and after delivery. 609 36

Plasma concentration of beta-endorphin was observed during labor in 16 women and correlated with pain assessed subjectively using pain scores. Ten women did not receive any medication during the follow-up. A concomitant increase in pain score and plasma beta-endorphin level was found with advancing labor. In the remaining six women, epidural anesthesia was used to relieve pain. During epidural anesthesia, plasma beta-endorphin levels and pain scores decreased concomitantly. The same effect was found after a repeated dose of the anesthetic. These findings showed a correlation between pain and the secretion of beta-endorphin during labor, but the mode of action of beta-endorphin remains unsolved.
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PMID:Pain and plasma beta-endorphin level during labor. 609 56

MIF-1 (Pro-Leu-Gly-NH2), a hypothalamic tripeptide, has been demonstrated to stimulate naloxone in antagonizing the effects of opioid peptides in a number of experimental systems including enkephalin-induced analgesia in the tail-flick assay, beta-endorphin induced hypothermia and hypomotility, deprivation-induced drinking, and analgesia in goldfish. MIF-1, however, has no effect upon the activity of enkephalins in the mouse vas deferens or enkephalin binding in the rat striatum. We have studied the interactions of MIF-1 with Leu5-enkephalin (Leu5-ENK) in the conscious, chronically instrumented dog. Although naloxone inhibits both the elevations of heart rate and blood pressure produced by IV Leu5-ENK in the conscious state and the depressions in these variables produced by Leu5-ENK after pentobarbital anesthesia, MIF-1 has no effect upon the Leu5-ENK response in either state. However, both naloxone and MIF-1 seem to raise mean arterial pressure in the conscious dog. These results indicate that MIF-1 does not act like naloxone in antagonizing the peripheral effects of Leu5-ENK and lend further support to the existence of mechanistic differences among opiate-mediated behavior, analgesia, and cardiovascular activity.
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PMID:MIF-1 does not act like naloxone in antagonizing the cardiovascular activity of leucine-enkephalin in the conscious dog. 613 37

Plasma beta-endorphin levels were studied before induction of general anaesthesia for caesarean section and during some phases of surgery. A very high increase of beta-endorphin occurred following induction of anaesthesia. However fifteen minutes after fetal extraction a tendency of the beta-endorphin levels to decrease was noted. Some medical treatment, such as antiasthmatic medication with glucocorticoids and beta-mimetic treatment for controlling uterine hyperactivity, seemed to interfere with pituitary response.
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PMID:Beta-endorphin levels and general anaesthesia for caesarean section. Preliminary report. 614 26


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