Beta-endorphin Concentrations Research Articles

Myocardial and peripheral concentrations of beta-endorphin before and following myocardial ischemia and reperfusion during coronary angioplasty.

There is substantial evidence indicating that endogenous opioid peptides are involved in the pathophysiology of myocardial ischemia and reperfusion. We measured the myocardial and peripheral concentrations of beta-endorphin before and following myocardial ischemia and reperfusion during coronary angioplasty. The results indicate that in patients with coronary artery disease, there was an augmented myocardial concentration of beta-endorphin. Moreover, there was an increased peripheral concentration of beta-endorphin following myocardial ischemia and reperfusion. The data support the previous notion that endogenous opioid peptides are involved in the pathophysiology of ischemic heart disease.

Determination of beta-endorphin plasma concentrations in surgical patients with acute abdominal pain

Abdominal pain and surgery, frequently associated with this kind of pain, modify plasma levels of stress-hormones and iniciates the response of endogenous analgetic system. The aim of this study was to determine serum concentration of beta-endorphine in patients with acute abdominal pain (n=12), which were surgically treated. Serum concentration of beta-endorphin was measured on five data points: before, during and after surgery. During abdominal surgery serum concentration of beta-endorphin was increased by 7% compared to preoperative period; in postoperative period the concentration continued to rise and remained increased within next hours. The maximal levels of beta-endorphine were not observed during, and immediately after surgery. Postoperatively, between 6 and 8 p.m. on the day of surgery, maximal level of beta-endorphin was noted, which was even ten times higher than to preoperative value. Plasma level of beta-endorphin fell to the baseline values 24 hours after surgery. In conclusion, abdominal surgery induces a postponed (delayed) increase in serum beta-endorphine levels, which are associated with modulation of preoperative, intraoperative and postoperative pain perception.

Mobilization of Opioid-containing Polymorphonuclear Cells by Hematopoietic Growth Factors and Influence on Inflammatory Pain

Leukocytes can control inflammatory pain by secretion of opioid peptides, stimulated by cold-water swimming or local injection of corticotropin-releasing factor, and subsequent activation of opioid receptors on peripheral sensory neurons. This study investigated whether mobilization of polymorphonuclear cells (PMN) by granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) enhances immigration of opioid-containing PMN and peripheral opioid analgesia in rats with Freund complete adjuvant-induced hind paw inflammation. In circulating PMN of rats treated with G-CSF+SCF and sham-treated rats, opioid peptide content was measured by radioimmunoassay. Expression of adhesion molecules (CD62L, CD49d, CD18), in vitro migration in the Boyden chamber, and infiltrating leukocytes were analyzed by flow cytometry. Chemokine messenger RNA transcription was quantified by LightCycler polymerase chain reaction. Paw pressure threshold was measured at baseline, after cold-water swimming, and after injection of corticotropin-releasing factor. G-CSF+SCF treatment increased circulating PMN (11-fold, P < 0.05). Mobilized PMN had decreased content of beta-endorphin but not of Met-enkephalin per cell, down-regulation of CD62L, up-regulation of CD49d (but no change in CD18), and reduced migration toward higher chemokine concentrations (all P < 0.05). In the paw, one of four chemokine messenger RNAs was significantly expressed during the first 2 h of inflammation (P < 0.05), immigration of PMN and opioid-containing cells was slightly increased (1.5-fold, P < 0.05), and baseline paw pressure threshold, as well as paw pressure threshold increases induced by corticotropin-releasing factor and cold-water swimming, were unchanged (P > 0.05). G-CSF+SCF mobilized circulating opioid-containing PMN but had a minor influence on cell migration and peripheral analgesia, probably because of the low expression of chemokines in the inflamed paw and one of the decreased beta-endorphin content in PMN.

Music as adjuvant therapy for coronary heart disease. Therapeutic music lowers anxiety, stress and beta-endorphin concentrations in patients from a coronary sport group

In a study with coronary patients it was estimated that music is able to lower stress and fear and contributing to relaxation in spite of physical exercise. 15 patients (13 male, two female, mean age 62,2 +/- 7,6 years) of a coronary sport unit were listening to an especially composed relaxation music while training their common heart-frequency adapted exercises. Before the exercises and after listening to music blood pressures were measured and blood was collected for determination of beta-endorphin. Simultaneous to blood collection the participants had to perform two psychometric test: the perceived stress experience questionnaire (PSQ) of Levenstein to measure the graduation of subjective perceived stress and the state-anxiety inquiry (STAI) of Spielberger as an indicator of coping. To practice the trial ("test trial"), the whole protocol was performed one week prior to the mean trial, but without listening to music and without blood collections and blood pressure measurements. In the test trial without music there were no significant changes in PSQ-data. In the mean trial, under the influence of music, values in the section "worries" decreased as a sign of lower worries (26.6 versus 27.6; p = 0.039). STAI-values were significantly lower as a sign of reduced fear after listening to music (31 versus 34; p = 0.045). beta-endorphin concentration (10.91 microg/l versus 15.96 microg/l, p = 0.044) and systolic blood pressure (130 mmHg versus 140 mmHg; p = 0.007) decreased significantly after listening to music. Regarding worries and fear, patients seemed to benefit by the intervention of music. beta-endorphin was lowered significantly after music despite physical activity.

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.

Beta-endorphin concentration after administration of sucrose in preterm infants.

Sucrose is an effective analgesic for procedural pain in preterm infants. It has been hypothesized that its analgesic effects are mediated by the release of endogenous opioid neurotransmitters such as beta-endorphin. To determine whether intraoral administration of sucrose was associated with an increase in serum beta-endorphin concentrations in preterm infants with a gestation period less than 29 weeks who were not exposed to a painful stimulus. We performed a prospective open-label study in preterm infants admitted to 2 tertiary neonatal intensive care units. Each infant received a single dose of 30% sucrose intraorally during a 1- to 2-minute period. A blood sample was obtained using an indwelling arterial catheter to determine beta-endorphin concentration immediately before and 2 to 5 minutes after the commencement of sucrose administration. We enrolled 11 preterm infants with a mean +/- SD gestational age of 27.2 +/- 0.9 weeks and a mean +/- SD birth weight of 1018 +/- 238 g (1.02 +/- 0.24 kg) at a mean +/- SD postnatal age of 3.0 +/- 2.5 days. The mean +/- SD beta-endorphin concentration before and after sucrose administration was 60.4 +/- 30.5 pg/mL and 57.4 +/- 22.4 pg/mL, respectively (P =.45). No adverse events were observed during the study procedures. Intraoral administration of sucrose in preterm infants did not lead to an increase in serum beta-endorphin concentrations at a point in time when the analgesic effects of sucrose were presumed to be present.

Immunity and beta-endorphin concentrations in hypothalamus and plasma in rats with steroid-induced polycystic ovaries: effect of low-frequency electroacupuncture.

The human endocrinological disorder polycystic ovary syndrome (PCOS) is a common cause of reproductive failure. Even though the cause of PCOS is unknown, hormone and immune disturbances as well as hyperactivity in the sympathetic nervous system are likely to be involved in the pathogenesis of the disease. The present study was undertaken to elucidate if rats with estradiol valerate (EV)-induced polycystic ovaries (PCO) have altered beta-endorphin concentrations in the hypothalamus and in plasma and if they have alterations in circulating immune cell populations and the activity. Repeated low-frequency (2 Hz) electroacupuncture (EA) treatments are known to modulate the release of beta-endorphin, immune responses, and the activity in the autonomic nervous system. We therefore also investigated the effect of EA treatments on the beta-endorphin and the immune systems. Low-frequency EA was given 12 times, 25 min each, over 30 days starting 2-3 days after i.m. injection of EV. The beta-endorphin concentrations in the hypothalamus and in plasma as well as the frequencies of CD4+ T cells and CD8+ T cells were significantly lower in EV-injected control rats as compared to oil-injected control rats. Repeated EA treatments in EV-injected rats significantly increased beta-endorphin concentrations in the hypothalamus. In conclusion, these findings show that both the beta-endorphinergic and the immune system are significantly impaired in rats with steroid-induced PCO and that repeated EA treatments can restore some of these disturbances.

Dietary exposure to genistein increases vasopressin but does not alter beta-endorphin in the rat hypothalamus.

Genistein is a plant-derived estrogenic isoflavone commonly found in soy-based products such as soymilk and soy-based dietary supplements for treating menopausal symptoms, for example. Vasopressin is a neurosecretory nonapeptide synthesized primarily in neurons of the hypothalamus and secreted into the bloodstream from the posterior lobe of the pituitary. The endogenous opiate peptide beta-endorphin is synthesized both in neurons of the hypothalamus and in pituitary cells, primarily of the neurointermediate lobe. It has been reported that exposure to 17beta-estradiol or diethylstilbesterol increased the vasopressin content of the hypothalamus, and that estradiol valerate selectively damages hypothalamic beta-endorphin-containing neurons. Since little was known of the potential effects of estrogenic endocrine-disruptor compounds on hypothalamic neuropeptides, we fed Sprague-Dawley fetuses from day 7 in utero until sacrifice at postnatal day 77, with either a control diet (<1 ppm) or an experimental diet containing 25, 250, or 1250 ppm of genistein. We then conducted ELISA assays for hypothalamic content of both beta-endorphin and vasopressin immunoreactivity. Whereas there were no statistically reliable effects of dietary genistein on hypothalamic beta-endorphin content, vasopressin levels were significantly elevated in the 1250-ppm genistein group (p < 0.05). Elevated vasopressin levels may be associated with fluid balance, altered blood pressure, and cardiovascular effects. These data are consistent with the known actions of estradiol and may serve to explain our finding in a previous study that estrogenic endocrine-disruptors such as genistein increased sodium preference in rats exposed through their diet.

Interaction among beta-endorphin, nitric oxide and prostaglandins during ovulation in rats

The aim of this study was to investigate the relationship between beta-endorphin and nitric oxide (NO) during the ovulatory process in rats. Immature rats were treated with equine chorionic gonadotrophin-hCG to induce ovulation. An intrabursal injection of beta-endorphin stimulated nitric oxide synthase (NOS) activity. This effect was completely reversed when naltrexone was co-injected with beta-endorphin. The stimulatory action of beta-endorphin on NOS activity was studied to determine whether it was exerted via prostaglandins. Treatment with prostaglandin E(2) (PGE(2)) completely reversed the beta-endorphin-induced stimulation of NOS activity. Moreover, intrabursal injection of meloxicam, an inhibitor of cyclooxygenase 2, increased NOS activity, but this effect was not altered by co-injection with beta-endorphin. The presence of both endothelial NOS (eNOS) and inducible NOS (iNOS) in the ovary at 10 h after hCG treatment was studied by western blot analysis. Local administration of beta-endorphin inhibited the expression of eNOS protein, whereas expression of iNOS protein was not detectable. Ovarian beta-endorphin content was diminished at 10 h after hCG injection. Treatment with prostaglandin synthesis inhibitors in vivo augmented the ovarian beta-endorphin content. In conclusion, these results indicate that beta-endorphin stimulates the activity of ovarian NOS indirectly by inhibiting prostaglandin production.

Interaction among beta-endorphin, nitric oxide and prostaglandins during ovulation in rats

The aim of this study was to investigate the relationship between beta-endorphin and nitric oxide (NO) during the ovulatory process in rats. Immature rats were treated with equine chorionic gonadotrophin-hCG to induce ovulation. An intrabursal injection of beta-endorphin stimulated nitric oxide synthase (NOS) activity. This effect was completely reversed when naltrexone was co-injected with beta-endorphin. The stimulatory action of beta-endorphin on NOS activity was studied to determine whether it was exerted via prostaglandins. Treatment with prostaglandin E(2) (PGE(2)) completely reversed the beta-endorphin-induced stimulation of NOS activity. Moreover, intrabursal injection of meloxicam, an inhibitor of cyclooxygenase 2, increased NOS activity, but this effect was not altered by co-injection with beta-endorphin. The presence of both endothelial NOS (eNOS) and inducible NOS (iNOS) in the ovary at 10 h after hCG treatment was studied by western blot analysis. Local administration of beta-endorphin inhibited the expression of eNOS protein, whereas expression of iNOS protein was not detectable. Ovarian beta-endorphin content was diminished at 10 h after hCG injection. Treatment with prostaglandin synthesis inhibitors in vivo augmented the ovarian beta-endorphin content. In conclusion, these results indicate that beta-endorphin stimulates the activity of ovarian NOS indirectly by inhibiting prostaglandin production.

Heavy load exercise induced dysfunction of immunity and neuroendocrine responses in rats

To determine whether immunity and neuroendocrine system is altered by different loads of exercise training in rats, eight-week-old male Sprague–Dawley rats were randomly assigned to one of the three groups: 1) cage control group (CCG); 2) moderate load training (MLT) (swimming at the intensity of 1.4 m/sec water flowing for 60 min per day); 3) heavy load training (HLT) (swimming at the intensity of 1.8 m/sec water flowing for 120 min per day). MLT and HLT rats were assigned to swim for 6 days per week for total of 6 weeks. All rats were sacrificed 36 h after their last training session. Splenocytes were pooled for assay of cell proliferation and neuropeptide contents in the hypothalamus, hypophysis and plasma were determined by radioimmunoassay while glucocorticoid specific binding in intact thymus was measured by radioligand binding assay. All rats were weighed weekly. The results showed that after 6-week training, rat splenocyte proliferation in response to Con A and LPS decreased in HLT rats compared with MLT and CCG rats. In addition, the contents of beta-endorphin, dynorphin A, arginine vasopressin and oxytocin in the hypothalamus, hypophysis and plasma were altered by HLT, as shown by increased plasma concentration of glucocorticoids and decreased glucocorticoids specific binding in intact thymus compared with MLT and CCG. Furthermore, a decreased body mass in HLT rats has been observed. The body mass of HLT rats was significantly lower than that in CCG and MLT rats at the end of the swimming training period. These data suggest that 6-week heavy load training induces the dysfunction of immunity and neuroendocrine responses, which might be one of the underlying mechanisms of immune dysfunction in overtraining.

Fat-tailed sheep traits as affected by docking.

The literature mostly indicates that docking fat-tailed lambs initially reduces growth but that post-weaning growth and feed conversion efficiency then increase. The amount of fat deposited, the total separable lean meat to fat ratio and the meat quality all increase, while the percentage of bone in the carcase either decreases or does not change in the carcases of the docked lambs. Wool growth and characteristics are, in general, not affected and reproductive traits in ewes and lambs are improved by docking. The rectal temperature, respiration rate and pulse rate are decreased following docking. The concentrations of immunoreactive beta-endorphin and cortisol in the plasma and the incidence of foot stamping and restlessness, as indicators of stress, increase after docking. Other constituents of the blood are not significantly altered following docking or by the methods of docking. Docking of fat-tailed sheep using rubber rings at one day of age can be recommended.

Differences in the Responses of the Pituitary β‐Endorphin and Cardiovascular System to Ethanol and Stress as a Function of Family History

Background Genetic and environmental factors, such as stress, are important for the initiation and maintenance of heavy drinking, whereas β‐endorphin may be important in controlling alcohol consumption. These studies investigated the response of pituitary β‐endorphin to stress and the effect of alcohol on the stress response in subjects at low (LR) and high (HR) risk of alcoholism, as determined from their family history.Methods Twenty LR and 20 HR subjects were exposed to stress 30 min after ingestion of either a placebo or an alcohol drink. Plasma β‐endorphin was measured before and for 4 hr after the drink. Changes in the concentration of plasma β‐endorphin after ingestion of the placebo or alcohol drink alone served as controls to compare the stress‐induced changes. Pulse and diastolic and systolic blood pressure were also measured.Results HR subjects presented higher baseline values of pulse and systolic blood pressure and lower plasma β‐endorphin than LR subjects. Stress induced a small increase in cardiovascular activity, whereas alcohol induced a stronger stimulation. Alcohol before stress did not prevent the stress‐induced increase in cardiovascular activity. Stress, but not alcohol, increased the plasma β‐endorphin concentration. LR subjects presented a higher stress‐induced increase in plasma β‐endorphin and a faster recovery than HR subjects. Alcohol before stress attenuated the stress‐induced increase in plasma β‐endorphin in both LR and HR subjects. This attenuation was stronger in LR subjects.Conclusions Thus, there are differences in the response of β‐endorphin to stress and the effect of ethanol on stress responses as a function of a family history of alcoholism.

Beta-Endorphin Concentration after Administration of Sucrose in Preterm Infants

Beta-Endorphin Concentration after Administration of Sucrose in Preterm Infants

Cutaneous analgesic, respiratory and cardiovascular effects, and beta-endorphin concentration in CSF and plasma of horses after electro-acupuncture

We tested the hypothesis that electro-acupuncture (EAP) can activate the horse's pain modulation system (pituitary or brain stem) to release beta-endorphin in spinal fluid and plasma which provides pain relief in horses. Eight adult healthy mares (510 ± 40 kg) were used in a randomized-crossover design study of 2 hours of EAP (test) and needle placement without electrical stimulation (sham-controls) with at least 3 weeks between experiments. Catheters were aseptically placed in the lumbar subarachnoid space, left carotid artery, and jugular vein of mares, using local anesthesia (2% lidocaine). Cerebrospinal fluid (3 mL) and venous blood (10 mL) were collected for radioimmunoassay of beta-endorphin (Tejwani et al., Life Sci. 1985). Arterial blood pressure, blood pH, PO2, PCO2, PCV, and TS concentrations were determined. Hwato acupuncture needles (28 gauge, 12.5 cm) were inserted at BL 18, 23, 25, and 28 on both sides of the spinal column of mares and were stimulated by an EAP stimulator (ITO IC 4107) using 15 and 30 Hz alternating frequencies, 4 V, 1 mA, and 0.1 ms biphasic square pulses in the test mares. Nociceptive skin pain threshold was measured by skin twitch reflex latency (STRL) and avoidance to radiant heat (48.5 °C cut-off) at the paralumbar fossa. Numerical scores of STRL, sedation, ataxia, respiratory and cardiovascular function, and beta-endorphin concentration in CSF and venous plasma were determined before (time 0), and 30, 60, 90, and 120 minutes after beginning and cessation of EAP and sham-controls. Two-way anova with repeated measures and Dunnett's post test were used. EAP significantly (p < 0.001) increased STRL [12.4 ± 2.1 seconds (mean ± SD) at baseline; 17.3 ± 2.2 seconds at 2 hours after EAP] and concentration of CSF beta-endorphin [17.5 ± 3.9 pg mL−1 (mean ± SD) at baseline; 26.1 ± 6.2 pg mL−1 at 2 hours after EAP], and minimally affected behavior and respiratory and cardiovascular systems of adult mares during and after the 2 hour-testing period.

Neuroendocrine effects of raloxifene hydrochloride in postmenopausal women

Raloxifene is a selective estrogen modulator able to exert an estrogen-like action on some target tissues and a specific antiestrogenic action on the uterus and breast. In ovariectomized rats, it has been shown to stimulate the beta-endorphin and allopregnanolone concentrations of the anterior and neurointermediate pituitary lobes, the hypothalamus and the hippocampus. The present study aimed to evaluate, in 12 healthy postmenopausal women, the effect of 60 mg/day raloxifene hydrochloride administration for 6 months on plasma beta-endorphin and allopregnanolone levels, and on the dynamic changes of both beta-endorphin and allopregnanolone secretion after the administration of: (1) clonidine, an alpha 2-presynaptic adrenergic agonist; (2) naloxone, an opioid receptor antagonist; and (3) fluoxetine, a serotonin selective reuptake inhibitor. The administration of raloxifene significantly increased both circulating beta-endorphin and allopregnanolone concentrations, at both the third and sixth months of treatment (p < 0.01). Clonidine, fluoxetine and naloxone administration before therapy was not able to stimulate the release of beta-endorphin, but the response was completely restored after raloxifene administration. Before therapy, clonidine and naloxone tests were accompanied by a significant rise in allopregnanolone secretion; the same changes were observed after raloxifene administration, but with significantly higher allopregnanolone concentrations at each time considered. While the fluoxetine test before therapy failed to increase the release of allopregnanolone, the same test after 6 months of raloxifene administration was characterized by a significant release of allopregnanolone at 60 and 90 minutes. The present data indicate that raloxifene has an estrogen-like effect on neuroendocrine pathways in postmenopausal women.

Opioid Peptide–expressing Leukocytes

Inflammatory pain can be effectively controlled by an interaction of opioid receptors on peripheral sensory nerve terminals with opioid peptides released from immune cells upon stressful stimulation. To define the source of opioid peptide production, we sought to identify and quantify populations of opioid-containing cells during the course of Freund's complete adjuvant-induced hind paw inflammation in the rat. In parallel, we examined the development of stress-induced local analgesia in the paw. At 2, 6, and 96 h after Freund's complete adjuvant inoculation, cells were characterized by flow cytometry using a monoclonal pan-opioid antibody (3E7) and antibodies against cell surface antigens and by immunohistochemistry using a polyclonal antibody to beta-endorphin. After magnetic cell sorting, the beta-endorphin content was quantified by radioimmunoassay. Pain responses before and after cold water swim stress were evaluated by paw pressure thresholds. In early inflammation, 66% of opioid peptide-producing (3E7+) leukocytes were HIS48+ granulocytes. In contrast, at later stages (96 h), the majority of 3E7+ immune cells were ED1+ monocytes or macrophages (73%). During the 4 days after Freund's complete adjuvant inoculation, the number of 3E7+ cells increased 5.6-fold (P < 0.001, Kruskal-Wallis test) and the beta-endorphin content in the paw multiplied 3.9-fold (P < 0.05, Kruskal-Wallis test). In parallel, cold water swim stress-induced analgesia increased by 160% (P < 0.01, analysis of variance). The degree of endogenous pain inhibition is proportional to the number of opioid peptide-producing cells, and distinct leukocyte lineages contribute to this function at different stages of inflammation. These mechanisms may be important for understanding pain in immunosuppressed states such as cancer, diabetes, or AIDS and for the design of novel therapeutic strategies in inflammatory diseases.

Beta endorphin concentrations in human milk.

The source and regulatory mechanisms that elevate beta-endorphin (beta-EP) approximately twofold higher than circulating plasma levels in the colostrum of lactating mothers are still unknown, and no studies have examined beta-EP availability previously during maturation phases of human milk. Therefore, the aim of this study was to determine whether concentrations of beta-EP vary over time between colostrum, transitional, and mature breast-milk and to evaluate whether this depends on the method of delivery. Mothers of healthy full-term and pre-term newborn infants who planned to breast-feed their newborn infants were considered for this study. They were consecutively recruited in one of 3 groups of 14, according to delivery method: group 1, vaginal delivery at term (gestational age 40.2 +/- 0.3 weeks; birth weight, 3.48 +/- 0.09 kg); group 2, preterm vaginal delivery (gestational age, 35.6 +/- 0.3 weeks; birth weight, 2.49 +/- 0.08 kg); and group 3, at-term elective cesarean section (gestational age, 39.0 +/- 0.3 weeks; birth weight, 3.32 +/- 0.14 kg). Three consecutive breast milk samples were obtained on the fourth day after birth, before each mother's discharge, and thereafter on the 10th and 30th postpartum days, close to expression of the colostrum, transitional, and mature milk production phases, respectively, to test beta-EP concentrations (beta-Endorphin 125I RIA; INCSTAR Corporation, Stillwater, MN). Data are presented as mean +/- standard deviation. Statistical comparison of beta-EP concentration among the three lactating mother groups was performed using the Kruskal-Wallis nonparametric test. In addition, to test the hypothesis of a trend toward smaller values with time of beta-EP, the authors computed within each mother group a P value per trend (Kruskal-Wallis test) of beta-EP concentration averages on the 4th, 10th, and 30th days, respectively. Student's t test for independent samples was used for the analysis of the other data. The 0.05 significance level was used in the statistical analysis. All computations were made by computer. Colostrum beta-EP concentrations on the fourth postpartum day of group 1 and group 2 mothers who were delivered of a neonate vaginally, at term, or prematurely were significantly higher (P < 0.01) than colostrum levels of group 3 mothers who underwent cesarean section. Group 2 mothers who were delivered of a neonate vaginally and prematurely presented the highest beta-EP concentrations (P < 0.05), lasting until the transitional milk phase (10th day). No significant differences were found across all 3 groups of lactating mothers in mature milk (30th day) beta-EP concentrations. In addition, the beta-EP trend toward smaller values with time within each of the three groups on days 4, 10, and 30 was statistically significant (P < 0.01 per trend). It is hypothesized that elevated beta-EP concentrations in colostrum and transitional milk of mothers who were vaginally delivered of infants may contribute to postnatal fetal adaptation, to overcoming birth stress of natural labor and delivery, and at the same time to the postnatal development of several related biologic functions of breast-fed infants.

Hormonal response to surgical stress in schoolchildren.

To determine hormone concentrations (ACTH, cortisol, beta-endorphin) in children before and after surgery, to assess the correlation between any hormonal changes and to study the influence exercised on them by the severity of surgical stress and the elective/emergency nature of the surgery. Prospective cohort of 78 children (age= 10+/-2.6 years, range 6-13 years) undergoing elective or emergency surgery. Preoperative and postoperative (1 and 24 hours postoperation) plasma concentrations of ACTH, cortisol and beta-endorphin were determined in all children. The severity of surgical stress was evaluated as low (< 6) or high (> 6) according to the Oxford scale. Student's t-test was used to analyse hormonal changes and the influence of degree of surgical stress and elective/emergency character of the surgery, and Pearson's coefficient for correlations between hormonal values. p < 0.05 was regarded as significant. We observed a significant increase in hormonal concentrations one hour after surgery. ACTH and cortisol values normalised 24 hours after surgery, but beta-endorphin concentrations remained increased. There was a correlation between ACTH and beta-endorphin values both before surgery and one hour after. Operations with high surgical stress significantly increased cortisol concentrations one hour after surgery and beta-endorphin concentrations 24 hours after surgery. Patients selected for emergency surgery showed significantly higher concentrations of cortisol and ACTH both before and after surgery. Postoperative hormonal response among children of school age is characterised by increases in ACTH, cortisol and beta-endorphin one hour after surgery, and by high concentrations of beta-endorphin 24 hours after surgery. Cortisol is an index of surgical stress. Emergency surgery is associated with significant increases in ACTH and cortisol.

Labor Pain Effects on Colostral Milk Beta-Endorphin Concentrations of Lactating Mothers

β-Endorphin (β-EP) levels of colostral milk are approximately two-fold higher than in plasma of lactating women, in who concentrations peak at term, after the first and second stages of labor. We investigated the effect of labor pain and vaginal parturition on colostral β-EP concentrations (β-endorphin ¹²⁵I RIA, Incstar Corp., Stillwater, Minn., USA) of at-term nursing mother, in comparison to those having undergone elective cesarean section. Our results show that colostral milk β-EP concentrations of mothers who delivered vaginally are significantly higher on the 4th postpartum day (6.0 ± 0.5 vs. 4.3 ± 0.4 pmol/l, respectively; p < 0.01) than colostral levels of mothers who underwent cesarean section. These data indicate the important influence of the labor process on the colostral opioid galactopoiesis. It is suggested that labor and parturition pain may increase colostral milk β- EP concentrations of lactating mothers in order to help the newborn overcome the stressful perinatal events of natural labor and delivery.