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)

The effect of the supplementation of nitrous oxide-oxygen anaesthesia with either fentanyl 15 micrograms kg-1 or 0.5% halothane on the beta-endorphin, ACTH, glucoregulatory hormonal and metabolic response to pelvic surgery was investigated. Fentanyl inhibited the increases in circulating beta-endorphin, ACTH, growth hormone, cortisol and glucose concentrations found in the patients receiving halothane. Changes in circulating beta-endorphin concentrations during surgery probably reflect alterations in pituitary secretion and appear to have no major metabolic effects. The suppression of pituitary secretion persisted for at least 4 h after the start of surgery.
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PMID:Fentanyl and the beta-endorphin, ACTH and glucoregulatory hormonal response to surgery. 295 4

The effects of an i.v. infusion of synthetic human beta-endorphin on the hormonal, metabolic and cardiovascular responses to surgery were investigated in female patients undergoing pelvic surgery. A beta-endorphin infusion (2 micrograms/kg as a bolus at induction of anaesthesia + 10 micrograms/kg/h for the first hour of surgery) increased plasma beta-endorphin immunoreactivity to values at least 100-fold greater than those seen during surgery in a control group of patients. In spite of this massive increase the only significant findings were a transient augmentation of the expected hyperglycaemic response and increased plasma glucagon values. There were no significant changes in ACTH, GH, insulin and cortisol secretion, in blood concentrations of lactate or glycerol, or in cardiovascular variables. Complete dissociation between plasma and cerebrospinal fluid concentrations of beta-endorphin was found even when plasma values exceeded 10,000 pmol/l in the presence of anaesthesia and surgery. These results show that the increase in circulating beta-endorphin immunoreactivity associated with clinical stress states are unlikely to modulate the associated hormonal, metabolic and cardiovascular changes.
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PMID:Beta-endorphin infusion fails to modulate the hormonal and metabolic response to surgery. 295 7

There is growing experimental evidence that beta-endorphin immunoreactivity is raised by surgical stress in patients undergoing general anesthesia. As the assay methods employed to date did not allow to fully discriminate between beta-endorphin and its immediate precursor, beta-lipotropin, we have investigated in the present study plasma levels of these two peptides by separating them by chromatography on plasma extracts prior to radioimmunoassay in eighteen surgical patients under general anesthesia and eight under spinal anesthesia. Beta-lipotropin, but not beta-endorphin, plasma levels were found to be significantly elevated during surgery in the general anesthesia group, while no change was found in either peptide concentration in the spinal one. Cortisol plasma levels also increased significantly 90 minutes after the beginning of surgery, when they were positively correlated to beta-lipotropin ones. Although the sampling time we adopted may have prevented us from detecting an early peak of beta-endorphin during the first 30 minutes of surgery, the major component of the pituitary opioid response to surgical stress appears to be related to beta-lipotropin. This is in agreement with results of experimental work on various kinds of stress in animals and humans and seems to rule out a role for plasma beta-endorphin in post-operative analgesia.
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PMID:Beta-lipotropin is the major component of the plasma opioid response to surgical stress in humans. 296 Aug 67

Relief of discomfort during acute myocardial ischemia is usually accomplished with a narcotic analgesic. Because these medications may cause unpleasant symptoms and exert a possibly adverse hemodynamic effect, the availability of alternative analgesic medication would be advantageous. Nitrous oxide is a commonly used potent analgesic gas. Nitrous oxide has been used to relieve ischemic discomfort during myocardial infarction. The current study was undertaken to corroborate that data in a randomized, blinded, cross-over study and to begin to explore a mechanism for the analgesic effect. Twelve patients with typical ischemic chest discomfort and a suspected myocardial infarction were included in the study. Each patient received a 30-minute inhalation treatment of 30% nitrous oxide/70% oxygen and 30 minutes of 30% room air/70% oxygen. Patients were blinded to their treatment and were randomized to receive nitrous oxide first, then room air, or vice versa. A semiquantitative assessment of the severity of chest discomfort was made before, during, and at the conclusion of each treatment together with a measurement of plasma beta-endorphin levels using a venous blood sample. Eleven of the 12 patients reported a significant reduction in the intensity of their chest discomfort during the nitrous oxide inhalation, but none had pain relief during the control period. Beta-endorphin levels fell to a greater extent during the inhalation of nitrous oxide than during the control period (51% versus 26%; P less than .05). No significant adverse effects were noted and most patients slept during the nitrous oxide inhalation. It is concluded that nitrous oxide anesthesia is a superior method of pain relief in patients with ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrous oxide anesthesia in patients with ischemic chest discomfort: effect on beta-endorphins. 296 38

The concentration of beta-endorphin-like immunoreactivity (beta-ELIR) was determined in plasma and cerebrospinal fluid (CSF) of rats at various times following the implantation under Hypnorm anesthesia of a permanent cannula into the cisterna magna. Plasma beta-ELIR levels were highly increased immediately after the operation, and gradually returned to basal within 6 h. The beta-ELIR concentration in CSF followed a completely different pattern. It appeared to be rather stable during the first hour after the operation, was decreased at 2 h, and showed a marked increase 24 h after surgery. Two days after the surgery, beta-ELIR levels in CSF had decreased to a stable basal level which was maintained for at least 7 days. When at this stage animals were treated with Hypnorm, plasma beta-ELIR was again highly increased 30 min and not 24 h after injection, but no changes were found in the beta-ELIR concentration in CSF. These data indicate that implantation of a cannula into the cisterna magna induces postoperative changes in the CSF levels of beta-endorphin that are detectable up to at least 24 h later. Moreover, the lack of correlation between CSF and plasma levels of beta-ELIR points towards differences in the regulation of brain and pituitary pro-opiomelanocortin cells.
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PMID:Differential effects of cisterna magna cannulation on beta-endorphin levels in rat plasma and cerebrospinal fluid. 296 46

Though acute nicotine administration results in increased blood pressure and heart rate, previous work has shown that chronic nicotine treatment does not result in significant hypertension. In fact, surprisingly it has been shown to produce hypotension. We performed the present experiments to further analyze the effects of chronic nicotine treatment. In untreated dogs (n = 7) under pentobarbital anesthesia (with adrenal hormone release measured directly by cannulation of the adrenolumbar veins) cumulative nicotine infusions (1-24 micrograms/kg/min i.v.) caused dose-dependent release of epinephrine (from 3.0 +/- 0.7 to 111 +/- 30 micrograms/kg/min) and norepinephrine (from 0.4 +/- 0.1 to 11.2 +/- 3.1). However, significant release of leu-enkephalin and met-enkephalin immunoreactivity was observed only with the highest nicotine infusion (24 micrograms/kg/min). In untreated conscious dogs (n = 12), nicotine test infusions (3 and 10 micrograms/kg/min), 15 min, yielded smoking relevant plasma nicotine levels and augmented heart rate, mean arterial pressure, plasma catecholamine levels, and adrenal epinephrine release. Plasma-enkephalin immunoreactivities were only marginally elevated with the higher nicotine test infusion. Chronic nicotine treatment (1.5 micrograms/kg/min s.c. for 5 weeks, n = 7), only transiently (first 1-2 weeks) augmented mean arterial pressure, heart rate, and epinephrine release, but during the plateau phase of treatment, hemodynamics and catecholamine parameters were identical to the pretreatment period. Acute responses of hemodynamics and catecholamines to nicotine test infusions declined progressively during chronic treatment, but the time course of this attenuation seemed not related to the reversal of the transient hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathoadrenal activity and sympathoinhibitory hormones during acute and chronic nicotine application in dogs. 297 78

Changes in serum levels of corticotrophin (ACTH), immunoreactive beta-endorphin, antidiuretic hormone and cortisol were compared in children undergoing minor surgery under either general anaesthesia with halothane or epidural anaesthesia by the caudal route. A rapid and major increase in hormone levels was observed under general anaesthesia but not under epidural anaesthesia.
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PMID:[Caudal epidural anesthesia in children. Study of endocrine changes]. 298 4

Little is known about adrenocortical function after coronary bypass surgery in which moderate to deep hypothermia and cardiopulmonary bypass are used particularly with intraoperative steroid administration. Therefore, we performed a pilot study in which immediately preoperative and 18-hour postoperative serum cortisol levels were determined in eight patients who received 1.0 to 1.5 gm of methylprednisolone intravenously during surgery; postoperative serum cortisol (3 +/- 1 microgram%) levels were lower than preoperative levels (15 +/- 3 microgram%, p less than 0.05). To determine the possible cause of these striking findings, the effects of moderate to profound hypothermia and cardiopulmonary bypass upon adrenocortical functioning were investigated without the influence of intraoperative steroid administration. Serum cortisol and aldosterone levels and their response to adrenocorticotropic hormone (ACTH) (Cortrosyn) were determined before coronary bypass surgery and at various postoperative intervals in seven patients. Postoperative cortisol and aldosterone levels increased markedly over their preoperative values, reaching a maximum at 6 to 12 hours (cortisol 16 +/- 8 vs 63 +/- 23 micrograms%, p less than 0.05, aldosterone 15 +/- 5 vs 51 +/- 22 ng%, p less than 0.05). Adrenal response to ACTH was normal preoperatively, during rewarming from hypothermia, and 18 hours, and 7 days postoperatively. In summary, normal adrenal responsiveness occurs after coronary bypass surgery, in spite of hypothermic cardiopulmonary bypass and the effects of anesthesia, and a single dose of methylprednisolone during surgery is associated with markedly lower serum cortisol levels and prevents the usual adrenal stress response to bypass surgery for at least 18 hours postoperatively.
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PMID:Adrenal function following coronary bypass surgery. 299 Jan 87

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

Opiates, like morphine, were long known to produce changes in blood pressure and cardiac functions. However, the nature of these changes are a subject of continuous controversy. The substantial differences in the opiate effects on the cardiovascular system is also apparent in more recent studies using enkephalins, beta-endorphin and dynorphins. The present review is aimed to indicate the source of the variations in the experimental data and analyze the relative contribution of different experimental factors to the observed effects of opiates and opioid peptides on the cardiovascular system. The major factors which contribute to the nature of the opioid effect on the cardiovascular system are: anesthesia, species, dose, site of action in the brain, respiratory changes and receptor specificity. However, the cardiovascular status per se is an important determinant of the opiates and opioid peptide effects on hemodynamic functions as indicated in states of hypertension and shock. A newly described factor is the plasticity of the opioid receptor system which changes its level and distribution pattern in different physiological and pathophysiological states. This review emphasizes the importance of utilization of highly specific ligands to opiate receptors administered to discrete brain areas in the conscious animal.
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PMID:The opioid system and central cardiovascular control: analysis of controversies. 300 75


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