Plasma beta-EP Research Articles

Effects of patient-controlled analgesia with small dose ketamine combined with morphine and the influence thereof on plasma beta-endorphin level in patients after radical operation for esophageal carcinoma

To evaluate the effects of patient-controlled analgesia (PCA) with small dose ketamine combined with morphine on analgesia and influence thereof on the plasma beta-endorphin (EP) level in the patients after radical operation for esophageal carcinoma. Thirty ASAI-II patients, aged 35-65, weighing 42-75 kg, with visual analogue score>or=3, undergoing elective radical operation for esophageal carcinoma under general anesthesia received intravenous morphine 2 - 3 mg were randomly divided into 2 equal groups: group m receiving morphine 0.02 mg.kg(-1).h(-1), and with group mk receiving morphine 0.02 mg.kg(-1).h(-1) combined with ketamine 0.08 mg.kg(-1).h(-1) for 50 h. In the course of treatment the patients received intravenous injection of morphine 2-3 mg when the VAS was >or=3. VAS was recorded 4, 8, 20, 24, and 48 h after operation. The amount of morphine used after operation, PCA button pressing times (effective/active), side effects, and vital signs including pulse, saturation of blood oxygen, respiratory rate, heart rate, and average arterial pressure were recorded. Central venous blood samples were collected when entering the operation room (T0), by the end of operation (T1), and 6 h (T2), 24 h (T3), and 48 h (T4) after operation respectively to examine the beta-endorphin level. During the period 4-48 h after operation the VAS scores of the group mk were significantly lower than those of the group m in activity state (all P<0.05) and were not significantly different those of the group m at resting state (all P>0.05). The total amount of morphine consumed and the actual PCA button pressing times were significantly less in the group mk than in the group m (both P<0.05). The incidence rates of nausea, vomiting, and pruritus of the group mk were all significantly lower than those of the group m (all P<0.05). There were not significant differences in the incidence rates of dreaming and pseudoesthesia between these 2 groups. All the vital signs were stable in the 2 groups. The plasma beta-EP levels at the time point T1 of these 2 groups were both significantly higher than those at T0 (both P<0.05). The plasma beta-endorphin levels at T2-4 of the group mk decreased gradually from the level at T1 to the level at T0, and the plasma beta-endorphin levels of the group m rapidly decreased from the level at T0 to the T0 level and remained at this level to the 48 h after operation. The combination of small dose of ketamine with morphine provides optimal analgesia with low side-effect rate and little effect on the plasma beta-EP level.

Detection of the levels of neuropeptides, ACTH and cortisol in the blood of patients with polymyositis/dermatomyositis and their significance.

Recent research has shown that the neuroendocrine system can regulate the function of the immune system and that ACTH and cortisol play important roles in maintaining the immune homeostasis. Polymyositis and dermatomyositis (PM/DM) are autoimmune diseases with unclear pathogeneses closely related with immune disorders, so we detected the levels of neuropeptide Y (NPY), beta-endorphin (beta-EP), calcitonin gene-related peptide (CGRP), adrenocoricotropic hormone (ACTH), and cortisol in blood of patients with PM/DM to investigate the relationship between these indices and the pathogenesis of PM/DM. The detection of NPY, beta-EP, CGRP, and ACTH concentrations in plasma and cortisol in serum of 28 cases of PM/DM was carried out using radioimmunoassay methods, and the results were compared with those of 20 normal controls. The levels of NPY in the plasma of PM/DM was significantly higher than those of the controls, while beta-EP, CGRP and ACTH were significantly lower than those of the controls, and cortisol was not significantly different before treatment. Linear correlation analysis indicated that NPY was significantly positively correlated with CPK, and beta-EP and CGRP were significantly negatively correlated with CPK. There were no significant correlations among cortisol ACTH, and CPK and no significant correlations between NPY, beta-EP, CGRP, ACTH, cortisol and age or duration of disease before treatment. After treatment for three months, NPY, beta-EP and CGRP tended to become normal and no longer significantly different from the control values. However, ACTH fell further and was significantly lower than the level before treatment. Therefore the increase in NPY and the decreases in beta-EP, CGRP, and ACTH in the plasma of PM/DM patients may be related to the pathogenesis of PM/DM.

Exploration on the effect and mechanism of Shenfu injection on resuscitation from general anesthesia

To investigate the effect and the mechanism of Shenfu injection (SFI) on the resuscitation from general anesthesia. Forty patients who received selective abdominal surgery with general anesthesia for 3-4 hrs and ASA grade I-II were divided into two groups, the trial group and the control group, 20 patients in each group. After being sent into the postanesthesia care unit (PACU), the trial group was treated with intravenous dripping of SFI 1.0 ml/kg and the control group was treated with intravenous dripping of equal volume of normal saline. All patients were observed in double blindly manner, the self ventilation recovery time, extubation time, the time of leaving PACU and their Glasgow coma scale (GCS) were recorded and compared. 2 ml of peripheral venous blood were taken to determine the plasma beta-endorphin (beta-EP) content at the time points of before (T1), 5 min (T2), 15 min (T3) and 30 min (T4) after dripping. The self ventilation recovery time, extubation time and time of leaving PACU in the trial group were all shorter than those in the control group (P < 0.01), the GCS in the trial group was better than that in the control group (P < 0.01). The plasma content of beta-EP raised gradually along the recovering of patients consciousness, as compared with the content before dripping (T1), it showed insignificant difference at time point T2 but significant difference at T3 and T4 comparison at the corresponding time point showed that the content at T1 and T2 were similar in the two groups (P > 0.05), but at T3 and T4, the content was higher in the trial group than that in the control group respectively (P < 0.01). SFI could accelerate the resuscitation after general anesthesia, the mechanism may be related with its action in raising plasma beta-EP level.

Plasma levels of beta-endorphin, adrenocorticotropic hormone and cortisol during early and late alcohol withdrawal.

Endogenous opioid peptides are thought to participate in the phenomena of alcohol tolerance and withdrawal. Since in the pituitary gland, beta-endorphin (beta-EP) and adrenocorticotropic hormone (ACTH) are produced from the same precursor molecule, pro-opiomelanocortin, it may be expected that alterations in plasma ACTH and cortisol levels should parallel changes in plasma beta-EP levels during alcohol withdrawal. The aim of the present study was to investigate the alterations of beta-EP, ACTH and cortisol secretion patterns in alcohol-dependent patients with heavy intake in the early withdrawal period and, if any, whether these changes remained stable on long-term withdrawal. Twenty-two hospitalized male patients (mean age +/- SD: 43.45 +/- 9.22 years, mean daily amount of alcohol +/- SD: 421.59 +/- 116.57 g) who were diagnosed to have alcohol withdrawal and 20 age-matched healthy men (mean age +/- SD: 38.35 +/- 7.63 years) were included in the study. Morning and night levels of plasma beta-EP, ACTH and cortisol were measured in the patients during the early (first week) and late (fourth week) withdrawal periods following alcohol cessation, and only once in the control subjects. It was found that both morning beta-EP and morning ACTH levels were reduced during both early and late withdrawals, whereas cortisol levels were increased in early withdrawal and normalized towards the late withdrawal period. The finding that beta-EP deficiency continued despite withdrawal symptoms subsiding in patients suggests that their beta-EP deficiency is independent of the withdrawal syndrome and that reduced beta-EP activity may be a trait contributing to alcohol craving.

Function and regulation of cholecystokinin octapeptide, beta-endorphin and gastrin in anorexic infantile rats treated with ErBao Granules.

To study the role of cholecystokinin octapeptide (CCK-8),beta endorphin (beta EP), and gastrin in an anorexic infantile rat model and no subsequent regulation of nose peptides by the Yunpi complex prescription ErBao Granule. We fed infantile rats with special prepared forage. A liquid extract of ErBao Granule was administered to the rats daily for 3 weeks, CCK-8, beta-EP, and gastrin concentrations in hypothalamus, gastric antrum, and plasma of the rats were measured by radioimmunoassay, and were compared with controls. Treatment of rats with ErBao Granule inhibited CCK-8 secretion and increased beta-EP and gastrin secretion. CCK-8 concentration in hypothalamus and plasma of model control group increased significantly and correlated negatively with food intake of models, respectively. beta-EP concentration in gastric antrum and plasma of model control group decreased significantly and showed a positive correlation with food intake of models, respectively. Hypothalamus concentration of beta-EP was similar in models and controls. Gastrin concentration in gastric antrum of models was lower than in the blank control group, and correlated positively to food intake of models. Finally, CCK-8 concentrations in plasma of rats showed a positive correlation with plasma beta-EP (r=-0.68, P<0.05). The increased plasma and hypothalamus concentration of CCK-8, decreased gastric antrum and plasma level of beta-EP, and decreased gastric antrum concentration of gastrin are associated significantly with the anorexia of infantile anorexic rat models produced by special for-age. ErBao Granule can reverse these changes, which may be the major mechanisms of ErBao Granule simulating feeding.

Maximal exercise transiently disrupts hormonal secretory patterns in standardbred geldings.

Basal concentrations of cortisol (CORT), beta-endorphin (beta EP), growth hormone (GH) and testosterone (T) and their disruption during 32 h of recovery after treadmill exercise were investigated in 4 geldings. Blood samples were collected from resting horses every 20 min between 0600-1000 and 1500-1900 h, and hourly between 1000-1500 h on 3 consecutive days. Treadmill exercise tests comprising 2 min intervals at 30, 50, and 70% VO2max then to fatigue at 100% VO2max were conducted between 1020-1130 h on Day 2. Blood was collected before, during and 15, 30, 60 and 90 min after exercise. Mean (Cav), peak (Cmax) and total (i.e. integrated) (Ctot) concentrations were calculated for CORT, beta EP and GH during the 20 min sampling sessions, and for CORT, beta EP, GH and T between 1000-1300 h on Days 1-3 (incorporating the samples during exercise on Day 2) and 1300-1900 h on Days 1-3. Cav, Cmax and Ctot for CORT, beta EP, GH and T were greater during exercise and recovery than in the same period on Day 1. Cav and Ctot values for plasma T during the 1300-1900 h period were significantly elevated on Day 2 and compared to Day 1 (P < 0.05), but there were no differences between Days 1 and 3 values for these variables. We concluded that plasma T concentration increases in response to maximal exercise in geldings, as does plasma CORT, beta EP and GH. Furthermore, maximal exercise disrupts basal plasma concentrations of CORT, beta EP and GH for up to 24 h and T for 26-32 h post exercise in geldings, therefore reflecting the minimum recovery periods required before evaluating normal, resting levels of these hormones in horses undergoing training.

Effect of TCM on plasma β-endorphin and placental endocrine in threatened abortion

To explore the effect of TCM on plasma beta-endorphin (beta-EP) and placental endocrine function in patients of threatened abortions (TA). Changes of plasma beta-EP, gonadotrophin releasing hormone (GnRH), human chorionic gonadotrophin (HCG), progesterone (P4) levels were measured with RIA in 40 cases of TA with a history of recurrent spontaneous abortion treated with Chinese herbal medicine for reinforcing Kidney and Qi, hemostasis and antiabortion. And the results were compared with those of normal early pregnant women and patients with incomplete abortion as control. The plasma beta-EP level in TA was significantly higher than that in normal pregnant women, P < 0.01. On the contrary, plasma GnRH, HCG and P4 were obviously lower in TA as compared with those of the normal cases, P < 0.01. After treatment, 36 of the 40 patients succeeded in the continuity of pregnancy, their symptoms of TA disappeared, and the above-mentioned four criteria measured at 10-12th week of gestation were similar to those of normal cases, P > 0.05. TCM treatment can regulate plasma beta-EP and placental endocrine function in threatened abortion.

Insulin, C-peptide, androgens, and beta-endorphin response to oral glucose in patients with polycystic ovary syndrome.

We examined the effects of an oral glucose load on plasma insulin, androgens, and beta-endorphin (beta EP) concentrations in patients carefully selected as having polycystic ovary syndrome (PCOS) and normal glucose tolerance. Our aim was to verify whether insulin resistance is a common feature of PCOS and to differentiate the metabolic abnormalities related to PCOS from those associated with obesity. Plasma immunoreactive insulin (IRI), C-peptide (C-PR), testosterone, androstenedione, dehydroepiandrosterone sulfate, ACTH, and beta EP responses to a 3-h oral glucose tolerance test (OGTT) were evaluated in 10 obese (OB-PCOS) and 10 nonobese (NO-PCOS) patients with PCOS and in 7 obese and 7 nonobese ovulatory controls. OB-PCOS and NO-PCOS did not differ significantly from weight-matched controls in the IRI response, but had a significantly higher C-PR response in terms of mean postglucose load levels and mean incremental areas. During OGTT, mean plasma levels of testosterone, androstenedione, and dehydroepiandrosterone sulfate declined in both PCOS groups as well as in controls, and no significant correlation between the plasma androgen and IRI or C-PR responses was found. The ACTH response in OB-PCOS and NO-PCOS was similar to that in controls, with a progressive decrease until 180 min. A similar decline in plasma beta EP was found in controls, whereas no change in plasma beta EP was observed in OB-PCOS and NO-PCOS. These findings indicate that independently of the presence of obesity, PCOS patients have enhanced insulin secretion in response to OGTT and show a peculiar pattern of changes in plasma beta EP.

Discrimination between beta-endorphin and beta-lipotrophin in human plasma using two-site immunoradiometric assays.

We wished to discriminate between the opioid peptide beta-endorphin (beta-EP) and its non-opioid precursor beta-lipotrophin (beta-LPH) in normal subjects and patients with ACTH-related disorders. We produced monoclonal antibodies to beta-EP and beta-LPH for the development of two-site immunoradiometric assays (IRMAs) which specifically quantitate beta-EP and beta-LPH. Samples were obtained from patients with a range of ACTH-related disorders and compared with 18 normal subjects. Peptide levels were also compared in six patients with Cushing's syndrome undergoing bilateral inferior petrosal sinus sampling with corticotrophin releasing hormone administration. In the beta-EP IRMA, antibody 6B2, specific for beta-EP 18-27, is radiolabelled and antibody 2E10, recognizing beta-EP 1-5, is coupled to Sephacryl S-300 as solid phase. The IRMA is specific for beta-EP (beta-LPH cross-reacts < 0.02%), has a detection limit of 1.4 +/- 0.7 pmol/l (n = 7) and has a within-assay coefficient of variation of < 10% between 4.9 and 1200 pmol/l. In the beta-LPH IRMA, antibody 6B2, which recognizes an epitope common to beta-LPH and beta-EP, is radiolabelled and paired with solid-phase antibody 5C11 which recognizes beta-LPH 39-56. The binding site of this antibody ensures that beta-EP cannot be measured in the beta-LPH assay. The detection limit is 0.8 +/- 0.1 pmol/l (n = 9) and the within-assay coefficient of variation is < 10% at concentrations 1.7-870 pmol/l. In normal subjects, beta-EP and beta-LPH levels were < 1.4-1.7 pmol/l (< 5-6 ng/l) and 2.5-6.7 pmol/l (29-77 ng/l) at 0930 h and < 1.4-1.7 pmol/l (< 5-6 ng/l) and 1.9-4.5 pmol/l (22-49 ng/l) at 1600 h, respectively. In patients with ACTH-related pathologies concentrations of beta-EP and beta-LPH paralleled those of ACTH. The ratio of beta-LPH:beta-EP in plasma varied between 3.2:1 and 38:1 in these patients demonstrating that beta-LPH is the major circulating peptide derived from the C-terminal of pro-opiomelanocortin in man. However, in two patients undergoing bilateral inferior petrosal sampling with corticotrophin releasing hormone for diagnosis of Cushing's disease beta-EP concentrations increased rapidly during the first 5 minutes of the test, resulting in a sharp decrease in the beta-LPH: beta-EP ratio. These results suggest that beta-EP is preferentially released in response to acute corticotrophin releasing hormone stimulation. It is concluded that two-site IRMAs for beta-EP and beta-LPH provide an easy approach to study the dynamic changes in processing of beta-LPH to beta-EP.

Acetyl‐L‐Carnitine Effect on Pituitary and Plasma β‐Endorphin Responsiveness to Different Chronic Intermittent Stressors

The aims of the present study were: 1) to compare the effect of two different chronic intermittent stressors i.e. cold-swimming versus ether, on the pituitary opioidergic system; 2) to evaluate the response of pituitary and plasma beta-endorphin (beta-EP) to an acute stress in chronically stressed rats; and 3) to evaluate the effect of acetyl-l-carnitine treatment (10 mg/day/rat per os at night) on pituitary and plasma beta-EP changes induced by two different types of chronic stress. The stressors were applied twice a day for 10 days. Rats were killed either before, during or after the last swimming or ether stress session. beta-EP was measured by radioimmunoassay in anterior pituitary and in neurointermediate lobe extracts and in plasma. The following observations were made: 1) Chronic intermittent cold-swimming stress increased anterior pituitary contents and plasma beta-EP levels; 2) both chronic intermittent cold-swimming stress and ether stress caused an increase of neurointermediate lobe beta-EP contents; 3) as in control animals, rats exposed to chronic intermittent swimming stress reduced pituitary beta-EP contents and raised plasma beta-EP levels in response to the last acute swimming stress; 4) in contrast to control animals, rats exposed to chronic intermittent ether stress did not show any significant response of the pituitary-plasma opioidergic system to the last acute ether session; 5) the acetyl-l-carnitine treatment counteracted the changes evoked by chronic intermittent cold-swimming stress on the pituitary and plasma beta-EP levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of different heavy-resistance exercise protocols on plasma beta-endorphin concentrations

To examine the changes of plasma beta-endorphin (beta-EP) concentrations in response to various heavy-resistance exercise protocols, eight healthy male subjects randomly performed each of six heavy-resistance exercise protocols, which consisted of identically ordered exercises carefully designed to control for the repetition maximum (RM) resistance (5 vs. 10 RM), rest period length (1 vs. 3 min), and total work (joules). Plasma beta-EP, ammonia, whole blood lactate and serum cortisol, creatine kinase, urea, and creatinine were determined preexercise, midexercise, immediately postexercise, and at various time points after the exercise session (5 min-48 h), depending on the specific blood variable examined. Only the high total work-exercise protocol [1 min rest, 10 RM load (H10/1)] demonstrated significant increases in plasma beta-EP and serum cortisol at midexercise and 0, 5, and 15 min postexercise. Increases in lactate were observed after all protocols, but the largest increases were observed after the H10/1 protocol. Within the H10/1 protocol, lactate concentrations were correlated (r = 0.82, P < 0.05) with plasma beta-EP concentrations. Cortisol increases were significantly correlated (r = 0.84) with 24-h peak creatine kinase values. The primary finding of this investigation was that beta-EP responds differently to various heavy-resistance exercise protocols. In heavy-resistance exercise, it appears that the duration of the force production and the length of the rest periods between sets are key exercise variables that influence increases in plasma beta-EP and serum cortisol concentrations. Furthermore the H10/1 protocol's significant challenge to the acid-base status of the blood, due to marked increases in whole blood lactate, may be associated with mechanisms modulating peripheral blood concentrations of beta-EP and cortisol.

Limited clinical usefulness of plasma corticotropin-releasing hormone, adrenocorticotropin and beta-endorphin measurements as markers of lung cancer.

We measured plasma corticotropin-releasing hormone (CRH), ACTH, beta-endorphin (beta-EP), and cortisol levels as possible tumor markers in a sequence of 103, randomly selected, patients with lung cancer but without the ectopic Cushing's syndrome and in 72 age- and sex-matched controls. Plasma CRH levels of cancer patients were similar to those of controls both in patients sampled in the morning or in the afternoon. On the other hand, plasma ACTH levels of cancer patients were significantly higher than control patients both in the morning and in the afternoon and showed a preserved circadian rhythm. However, about 35% of cancer patients sampled in the morning and about 60% of those sampled in the afternoon had ACTH levels within the 95% confidence interval (CI) of controls. Also plasma beta-EP levels were more elevated in cancer patients than controls in the morning but about 33% of them and about 80% of those sampled in the afternoon had beta-EP levels within the 95% CI of controls. Despite the higher plasma ACTH levels, cancer patients had cortisol plasma levels similar to controls with preserved circadian rhythm. In conclusion, although mean plasma ACTH and beta-EP were higher in patients affected by lung cancer, their measurements, as well as those of CRH, have practically no diagnostic value. Perhaps measurement of ACTH levels in the bronchial lavage may be more helpful.

Plasma beta-endorphin and adrenocorticotrophin in young horses in training.

A controlled period of submaximal exercise on a treadmill was used as a standardised stress test in 6 young horses to monitor the effects of training. Circulating plasma concentrations of immunoreactive beta-endorphin (IR beta-EP) were measured before, during and after the exercise period. The stress test was conducted on 3 occasions during an intensive training program lasting 14 weeks. In week 3 a marked increase in plasma IR beta-EP (P = 0.003) was demonstrated as a result of training, but by the last exercise test performed in week 9 no significant increase in plasma IR beta-EP concentrations could be detected. During the training period the basal concentrations of plasma IR beta-EP significantly decreased (P = 0.0059). Plasma adrenocorticotrophin (ACTH) did not increase during exercise, although there was a trend of decreasing basal plasma ACTH by the end of the training period. It was concluded that a standardised work test acted as a mild stress to unfit horses, but as the horses' fitness increased the hormonal response to exercise diminished. Basal plasma beta-EP concentrations were decreased with increasing fitness.

Resistance of beta-endorphin to dexamethasone inhibition in Parkinson's and Alzheimer's diseases.

The response of plasma beta-endorphin (beta-EP) to dexamethasone suppression was studied in 14 patients with Alzheimer's disease (AD), 14 patients with Parkinson's disease (PD), and 13 age-matched controls in order to evaluate whether an impairment of the opiate system is present in these neurodegenerative disorders. Basal circulating beta-EP was in normal range in all subjects, although the mean concentration was slightly reduced in the patients compared to controls. After 1 mg dexamethasone given at 11:00 p.m. the night before, plasma beta-EP concentration measured at 08:00 a.m. and 04:00 p.m. was not inhibited in AD and PD patients while it was significantly reduced in controls. Circulating ACTH and cortisol were similar in patients and controls and a normal inhibition of plasma cortisol after dexamethasone was observed in 13/14 AD and 12/14 PD patients. The resistance of beta-EP to dexamethasone inhibition is consistent with previous clinical and experimental data indicating a disorder of the opiate system in brain degenerative diseases.

Plasma Beta-Endorphin during Fasting in Man

To identify the effects of acute starvation on endogenous opioids in man, plasma beta-endorphin (beta-EP) was measured in 17 patients before, during and after fasting. Patients were assigned a posteriori into two groups: group A, comprised of 11 patients able to tolerate 5-7 days of fasting, and group B, comprised of 6 patients able to tolerate 10 days of fasting. Changes in plasma beta-EP, serum cortisol, circulating nutritional markers, and their relative levels were assessed on the 5th and 10th days of fasting, and on the 5th and 10th days of the refeeding period. Beta-EP had increased by the 5th day (group A: 4.74 +/- 0.42 to 6.91 +/- 0.65 pmol/l, p less than 0.01; group B: 3.60 +/- 0.48 to 5.14 +/- 0.22 pmol/l, p less than 0.05, and remained at 5.05 +/- 0.65 pmol/l on the 10th day (group B: 0.05 less than p less than 0.1) during fasting. Group B had lower levels of plasma beta-EP on the 5th day of fasting than group A (p less than 0.05). However, serum cortisol levels changed similarly in both groups. Plasma beta-EP showed no significant correlation with either the percentage of body weight lost or the body mass index (kg/m2) over this study period. These findings indicate that plasma beta-EP is elevated in the early phase of fasting, while not directly being associated with body weight changes. Plasma beta-EP is lower and less activated in subjects who are able to tolerate fasting for longer periods.

Plasma beta-endorphin and beta-lipotropin levels increase in well trained athletes after competition and non competitive exercise

Plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) levels were measured in 15 healthy trained marathon runners. These hormones were evaluated in two different conditions: 1-before (1h) and after a marathon race (n = 10); 2-before, during and after a prolonged (90 min) submaximal exercise (bicycle ergometer at 50% VO2 max) (n = 5). In these latter group plasma beta-EP and beta-LPH levels were measured every 15 min for 165 min. In all the athletes, both plasma beta-EP and beta-LPH levels were significantly higher after the end of the marathon race than in basal conditions (p less than 0.01). The prolonged exercise with bicycle ergometer significantly stimulated plasma beta-EP and beta-LPH levels. Starting 60 min after the beginning of the exercise, plasma beta-EP and beta-LPH levels resulted significantly higher than basal values until the end of the exercise (p less than 0.01 at 60, 75 and 90 min). These data confirming that marathon running is a potent stress stimulus, showed that the duration and related factors but not the work load may be considered critical in stimulating beta-EP and beta-LPH release during physical exercise.

Circulating Opioid Peptides During Thermal Stress

In the present study we have examined the response of endogenous opiates (beta-EP and Met-enk) and ACTH to a particular type of thermal stimulus such as sauna in 8 young healthy subjects. Sauna-induced hyperthermia resulted in an increase of plasma beta-EP and ACTH, but appeared to have no significant effect on circulating Met-enk. The different responses of ACTH, beta-EP and Met-enk to heat exposure indicate that hyperthermia represents a form of stress, which can trigger off a well-defined neuroendocrine reaction.

Lidocaine treatment of painful diabetic neuropathy and endogenous opioid peptides in plasma.

Intravenous infusion of lidocaine has a pain-relieving effect in patients with painful diabetic neuropathy. We measured plasma beta-endorphin (beta-EP), dynorphin immunoreactivity (DYN), and met-enkephalin (MET) before and after lidocaine infusion in 8 patients with painful diabetic neuropathy and in 10 controls. The pretreatment level of beta-EP and DYN was identical in the two groups. After lidocaine, beta-EP increased in diabetic patients from 3.4 to 5.5 pmol/L (median) (p less than 0.02) and in controls from 3.4 to 5.0 pmol/L (p less than 0.02). The concentration of DYN was stable, and MET was undetectable before and after lidocaine. Lidocaine reduced symptoms and pain score in diabetic patients was uncorrelated with the changes in beta-EP. Intravenous lidocaine increased plasma beta-EP and diminished complaints in patients with painful diabetic neuropathy.

Training responses of plasma beta-endorphin, adrenocorticotropin, and cortisol

The purpose of this study was to examine the effects of three different run training programs on plasma responses of beta-endorphin (beta-EP), adrenocorticotropin (ACTH), and cortisol to maximal treadmill exercise. Subjects were randomly assigned to one of three training groups: sprint intervals (SI) (N = 8), endurance (E) (N = 10), or combination (C) (N = 7). Training was monitored for 10 wk, and maximal treadmill exercise tests were administered pre-training and after 2, 4, 6, 8, and 10 wk of training. Blood samples were obtained (pre-training and after 10 wk) before, immediately after, and 5 and 15 min following the maximal exercise tests. All groups significantly (P less than 0.05) increased maximal oxygen consumption values at 8 and 10 wk of the training period. Significant exercise-induced increase in plasma beta-EP, ACTH, cortisol, and blood lactate were observed for both pre- and post-training tests in all training groups. The SI group demonstrated significant post-training increases in beta-EP, ACTH, cortisol, and 5 min post-exercise blood lactate concentrations in response to maximal exercise. No training-induced hormonal changes were observed for the E group. While exercise-induced increases were observed, the C group exhibited significant post-training reductions in plasma responses of beta-EP, ACTH, and blood lactate concentrations in response to maximal exercise. Still, resting and post-exercise increases in plasma cortisol concentrations were significantly higher in magnitude in the post-training test. Lactate was significantly correlated with beta-EP (r = 0.72), ACTH (r = 0.70), and cortisol (r = 0.64).(ABSTRACT TRUNCATED AT 250 WORDS)

Evidences for a dopamine-regulated peripheral source of circulating beta-endorphin.

Circulating beta-endorphin (beta EP) and beta-lipotropin (beta LPH) concentrations increase after the administration of acetylcholine or serotonin agonist drugs. In this study we examined the effect of dopamine receptor agonists and/or antagonists on plasma beta EP, beta LPH, cortisol, and PRL levels in normal subjects. Neither direct dopamine (DA) agonist drugs, DA (1 microgram/kg min for 120 min), bromocriptine (2.5 mg po), L-dopa (500 mg po) or an indirect DA agonist, nomifensine (200 mg po), significantly altered plasma beta EP and beta LPH levels. The administration of metoclopramide, a DA antagonist (10 mg iv), significantly increased plasma beta EP, beta LPH, PRL, and cortisol levels. This effect was completely reversed by pretreatment with L-dopa (500 mg po) and only partially antagonized by DA infusion. Domperidone (10 mg iv), a DA antagonist which does not cross the blood brain barrier, increased only plasma beta EP levels, an effect inhibited both by L-dopa and DA. After dexamethasone (2 mg/day for 2 days) domperidone still increased plasma beta EP and PRL levels. The concomitant increase of beta EP, beta LPH, and cortisol after metoclopramide suggests that endogenous DA inhibits the secretion of proopiomelanocortin-related peptides. Moreover, since domperidone increases only beta EP and this effect is not altered by dexamethasone, there may be a corticotropin-releasing hormone-independent source of circulating beta EP in humans, which is inhibited by DA.