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)

Concentration of beta-endorphin in relation to the mode of delivery and anesthesia was studied in maternal and umbilical cord plasma in 30 healthy women at term pregnancy. At elective cesarean section under epidural anesthesia, the mean maternal beta-endorphin level rose from 9.8 +/- 2.7 pmol/L (SE) before induction to 15.5 +/- 3.7 pmol/L at the time of delivery (P less than .02). Under general anesthesia the mean beta-endorphin level increased more, from 14.6 +/- 7.2 to 34.4 +/- 7.8 pmol/L (P less than .02), reaching the mean beta-endorphin value of the second stage of normal labor, 39.4 +/- 7.0 pmol/L. In the cord arterial and venous plasma, the mean beta-endorphin value was significantly higher after spontaneous labor (40.9 +/- 11 and 40.1 +/- 9.2 pmol/L, respectively) than at elective cesarean section under epidural (14.3 +/- 1.9 and 12.4 +/- 3.6 pmol/L, respectively) or general anesthesia (11.9 +/- 2.2 and 13.4 +/- 2.2 pmol/L, respectively). Thus cesarean section under general anesthesia proved to be more stressful for the mother than that under epidural anesthesia, when beta-endorphin release is used as the measure of stress. The mode of anesthesia did not seem to influence the plasma beta-endorphin level in the newborn infant. Normal delivery by vaginal route increased the release of beta-endorphin both to the maternal and the fetoplacental circulation.
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PMID:Beta-endorphin in maternal and umbilical cord plasma at elective cesarean section and in spontaneous labor. 293 62

Multiunit activity (MUA) of arcuate nucleus and cortical EEG were recorded in the regularly cycling female rats on the day of proestrous under urethane anaesthesia. The MUA was compared before and after injection of beta-endorphin in third ventricle. In some animals MUA increased after 30-40 min and persisted for 3-4 hr, in others MUA got inhibited within 5-10 min of injection of beta-Endorphin and effect lasted for 5-6 hr. There was no change in frontoparietal EEG activity. In another group of animals medial pre-optic responses (MPO) to stimulation of medial amygdala were tested before and after ventricular infusion of beta-endorphin. Most of the facilitatory MPO responses got blocked. These observations suggest the involvement of opioid receptors in the mediation of neuroendocrine control of preovulatory events through the amygdalo-preoptico-medial basal hypothalamic axis. There seems to be heterogeneity of beta-endorphin receptors in the arcuate nucleus.
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PMID:Effect of third ventricular injection of beta-endorphin on the electrophysiological responses of some regions of endocrine hypothalamus. 293 83

To explore the hypothesis that nitrous oxide stimulates the beta-endorphin system in vivo, rats were exposed to nitrous oxide/oxygen at variable concentrations for one hour. beta-Endorphin concentration at sites along the neuraxis functionally involved with analgesia was elevated in nitrous oxide-exposed animals. The increase in beta-endorphin concentration was statistically significant at nitrous oxide concentrations of 60 and 80%. This elevation of beta-endorphin levels depended on the concentration of nitrous oxide delivered rather than on the duration of exposure. With cessation of nitrous oxide anesthesia, beta-endorphin concentration returned to control levels within 30 minutes.
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PMID:Central beta-endorphin release and recovery after exposure to nitrous oxide in rats. 294 84

Immunoreactive beta-endorphin (ir-beta-END) concentrations were measured in the hypophysial portal plasma of the male rat under urethane anesthesia. On the basis of immunochemical studies and gel filtration chromatography it appears that ir-beta-END in rat hypophysial portal plasma is primarily beta-endorphin (beta-END) and not beta-lipotropin (beta-LPH). In addition, much of the ir-beta-END in portal plasma may be of pituitary origin since acute hypophysectomy resulted in approximately an 80% decrease in the portal plasma concentration of ir-beta-END. Nevertheless, in anesthetized animals that had been hypophysectomized acutely, portal plasma concentrations of ir-beta-END were still 5 times those in systemic plasma, indicative of hypothalamic secretion of the peptide. The administration of morphine sulfate (3 mg/kg, i.v.) resulted in a decrease of ir-beta-END concentrations from 3,157 +/- 547 pg/ml to 1,044 +/- 250 pg/ml. This effect was blocked by naltrexone (1 mg/kg, s.c.) pretreatment. Capsaicin (10 micrograms), which, when infused into the lateral cerebral ventricle of the rat, has been shown to decrease the amount of beta-END in the hypothalamus, but not elsewhere in the central nervous system, selectively decreased the concentration of ir-beta-END in portal plasma without changing systemic ir-beta-END concentrations. These studies indicate that ir-beta-END in portal plasma is probably beta-END which is derived from neurons in the hypothalamus. Moreover, it is concluded that the regulation of the release of ir-beta-END from these neurons involves opiate receptor mechanisms. The inhibitory influence of opiates on ir-beta-END secretion may be indicative of a classical feedback regulation of ir-beta-END-containing neurons.
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PMID:Morphine or capsaicin administration alters the secretion of beta-endorphin into the hypophysial portal vasculature of the rat. 294 26

Plasma cortisol, beta-endorphin immunoreactivity (PBEir) and arginine vasopressin (AVP) responses during and after the continuous infusion of fentanyl or alfentanil were studied in 19 patients undergoing coronary artery bypass grafting (CABG). Plasma cortisol concentration decreased significantly in both groups during the anaesthesia and surgery before cardiopulmonary bypass (CPB); an increase was evident during CPB in both groups, but a statistically significant increase was not observed during the rest of the study, including the awakening from anaesthesia. PBEir increased with both opiates immediately after initiation of CPB and remained so during the rest of the study. There were no significant changes in plasma AVP concentrations during anaesthesia and surgery. After discontinuation of opiate infusions, an increase in AVP concentration commenced earlier in the alfentanil group than in the fentanyl group. At awakening from anaesthesia, a significant correlation was observed between log plasma AVP concentration and systemic vascular resistance. It is concluded that, with continuous fentanyl and alfentanil infusions in a total dose relationship of 1:13 in patients undergoing CABG, cortisol and AVP responses to surgery and CPB can be suppressed. However, during recovery from anaesthesia, the attenuating effect of alfentanil seems to wear off more rapidly than that of fentanyl. PBEir response to CPB and emergence from anaesthesia could not be prevented with either analgesic.
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PMID:Continuous infusion of fentanyl or alfentanil for coronary artery surgery. Effects on plasma cortisol concentration, beta-endorphin immunoreactivity and arginine vasopressin. 294 13

We have developed and validated a push-pull technique that allows focal perfusion of the ovary in unanesthetized freely moving rats. We have used this method to investigate the intraovarian secretion of catecholamines (dopamine, norepinephrine, epinephrine), oxytocin, beta-endorphin and gamma-amino-butyric acid (GABA) during the estrous cycle. Cycling animals were implanted with ovarian push-pull catheters and jugular vein catheters under ether anaesthesia on proestrus, estrus and diestrous Day 2. This procedure did not disrupt normal preovulatory release of prolactin and luteinizing hormone (LH). Thus, perfusion of the ovary and simultaneous monitoring of hormone levels in systemic blood in freely moving rats allow correlation of the temporal relationship of ovarian events with cyclic gonadotropin secretion. The results clearly indicate that a rise in ovarian norepinephrine occurs concomitant with the preovulatory surge in prolactin and LH. Ovarian beta-endorphin concentrations exhibit cyclic changes, whereas GABA release rates remain stable throughout the cycle. Oxytocin is secreted by ovarian tissue, and the secretion rate appears to be inversely related to prolactin. In view of the proposed involvement of ovarian nerves and particularly catecholamines in the process of follicular maturation and ovulation, our findings suggest a preovulatory activation of ovarian noradrenergic sympathetic neurons.
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PMID:Intraovarian secretion of catecholamines, oxytocin, beta-endorphin, and gamma-amino-butyric-acid in freely moving rats: development of a push-pull tubing method. 294 38

17 patients undergoing cholecystectomy in non-opiate general anaesthesia received tramadol (n = 7) or fentanyl (n = 10) for immediate postoperative pain relief using the on-demand analgesia computer (ODAC). Heart rate, blood pressure, and respiratory rate were monitored at half-hourly intervals during the 6-h trial period. Arterial blood was withdrawn at hourly intervals for blood gas analyses and beta-endorphin plasma level assays. Fentanyl and tramadol serum levels were determined prior to each on-demand bolus injection during the first 2 h of the study. At the end of the trial period, the quality of analgesia was assessed retrospectively using a visual analog scale. Mean opiate consumption was 0.53 +/- 0.1 mg for fentanyl and 412 +/- 11.6 mg for tramadol, resulting in an equipotency ratio of about 1:980 (relating to body wt., consumption/h, and pain score). No correlation was found between body wt.-based opiate requirements and pain score. Heart rate increased slightly but significantly under both opiates. Fentanyl produced a significant drop in mean arterial pressure by a maximum of 16%, while tramadol left mean arterial pressure unchanged. Respiratory rate, which was elevated initially, dropped significantly in both groups. Arterial pO2 and pCO2 were within the normal range throughout the observation period, reflecting the absence of respiratory side effects. Opiate blood levels showed major inter- and intraindividual variations (minimal and maximal levels for fentanyl ranged from 0.44-3.44 ng/ml, for tramadol from 272-1,900 ng/ml) and were thus poor predictors of the quality of analgesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of fentanyl and tramadol in pain therapy with an on-demand analgesia computer in the early postoperative phase]. 294 72

Neurotensin (NT) differentially altered ethanol-induced anesthesia as measured by duration of loss of righting response or by blood ethanol levels producing loss of righting response in mice (LS and SS) which were selectively bred for differences in response to ethanol. At doses of 5-500 ng i.c.v., NT increased ethanol sensitivity in SS mice, but not in LS mice, as measured by blood ethanol concentrations at loss of righting response. At higher doses, 0.5-10 micrograms i.c.v., NT enhanced the sensitivity of both SS and LS mice to ethanol-induced anesthesia. The hypothermic effect of ethanol determined at loss of righting response was not altered in either LS or SS mice at low doses of NT, but at higher doses NT enhanced ethanol-induced hypothermia in both lines of mice. The altered anesthetic sensitivity was specific for ethanol in that NT did not alter pentobarbital-induced sleep time in either LS or SS mice and halothane anesthesia was altered slightly only in LS mice. NT analogues, N-acetyl-NT8-13, and [D-Trp11]-NT but not NT1-8 enhanced the anesthetic action of ethanol in SS mice. Bombesin, cholecystokinin sulfate, substance P, [D-Trp8, D-Cys14]-somatostatin and corticotropin releasing hormone (CRF) were not effective in enhancing ethanol-induced anesthesia in LS or SS mice. CRF appeared to decrease ethanol sensitivity in LS but not in SS mice. Beta-Endorphin (beta-END) markedly increased the ethanol sensitivity of SS and to a lesser extent of LS mice at relatively high doses, e.g. 0.5-1.0 micrograms i.c.v. The results of the present study indicate that differences in brain sensitivity of LS and SS mice to ethanol may be mediated by genetic differences in NT systems. Likewise, NT, and probably beta-endorphin, may interact with other neurochemical processes that are involved in the mechanism of ethanol-induced anesthesia and that differ genetically in LS and SS mice.
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PMID:Neurotensin selectively alters ethanol-induced anesthesia in LS/Ibg and SS/Ibg lines of mice. 294 96

Recent evidence has suggested that a circadian rhythm exists for plasma beta-endorphin-like immunoreactivity. The purpose of the present study was to examine the long term effects of surgical trauma on plasma beta-endorphin dynamics. Blood samples for RIA were obtained from female baboons every 4 h for three 48-h periods: one beginning 1 week before surgical trauma, the second 30 min after surgical trauma, and the third 1 week after surgical trauma. Animals were subjected to laparotomy and 30-min anesthesia (n = 8), 5-min surgical trauma under 30-min anesthesia (low trauma; n = 8), or 20-min surgical trauma under 30-min anesthesia (high trauma; n = 8). Computer analysis of beta-endorphin levels as a function of clock time demonstrated a true preoperative circadian rhythm for all animals, with a mean of 87.9 pg/ml. In the immediate 48-h postoperative period, a postoperative alteration in circadian beta-endorphin dynamics occurred that was correlated with the severity of trauma. A disruption of circadian rhythms of plasma beta-endorphin occurred in the high trauma group only, in which it persisted for longer than 1 week after trauma. These studies establish a relationship between the alteration of circadian rhythmicity of plasma beta-endorphin-like immunoreactivity and the magnitude of trauma and injury.
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PMID:Prolonged disruption of plasma beta-endorphin dynamics after trauma in the nonhuman primate. 295 90

Modifying effects of epidural analgesia and general anesthesia on stress hormone release was studied during laparoscopy for in vitro fertilization (IVF). In 24 women follicle development was stimulated by clomiphene and gonadotropin treatment, and oocytes were collected by laparoscopy under epidural analgesia in 11 women and under fentanyl-supplemented nitrous oxide-oxygen anesthesia in 13. The plasma levels of immunoreactive beta-endorphin (ir beta-E), cortisol, and prolactin (PRL) did not change under epidural analgesia per se, but after the start of laparoscopy, increased release of all these stress hormones was observed. General anesthesia per se increased the release of PRL, whereas the release of cortisol and ir beta-E decreased, probably due to the effects of fentanyl and thiopentone. During the stress attributed to laparoscopy, significantly more ir beta-E and cortisol was released under epidural than under general anesthesia, whereas the release of PRL was more significant under general anesthesia. These results show that neither mode of anesthesia prevented the stress response to laparoscopy. In the subsequent midluteal phase, the mean plasma level of progesterone and the mean progesterone-estradiol ratio were significantly greater in the epidural than in the general anesthesia group, suggesting that the mode of anesthesia may have an effect on the luteal phase. The significance of this difference on the conception rate remained unsolved, however.
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PMID:Modifying effects of epidural analgesia or general anesthesia on the stress hormone response to laparoscopy for in vitro fertilization. 295 34


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