beta-endorphin and Chronic-Disease

In the present study, we demonstrated that repeated treatment with fentanyl, but not morphine or oxycodone, causes a rapid desensitization to its ability to block the hyperalgesia associated with the attenuation of mu-opioid receptor resensitization in mice in a chronic pain-like state. In contrast, no such effect was noted in beta-endorphin knockout mice under the chronic pain-like conditions. On the assumption that beta-endorphin might be released within the spinal cord under pain-like conditions, we further examined whether beta-endorphin could be responsible for a desensitization and resensitization of fentanyl under the chronic pain. In cultured cells, unlike morphine, fentanyl and oxycodone induced a robust mu-opioid receptor internalization and, in turn, its resensitization. In the presence of beta-endorphin, the internalized mu-opioid receptor induced by fentanyl, but not oxycodone, remained within the cytosolic component even after washing out. The findings suggest that beta-endorphin could attenuate the resensitization of mu-opioid receptors. This phenomenon may explain the high degree of tolerance to fentanyl that develops with hyperalgesia caused by a chronic pain-like state.

Topics: Analgesics, Opioid; Animals; beta-Endorphin; Chronic Disease; Disease Models, Animal; Drug Tolerance; Fentanyl; Humans; Mice; Morphine; Oxycodone; Pain; Receptors, Opioid, mu

It is well established that cholecystokinin (CCK) reduces the antinociceptive effect of opioids. The level of CCK and CCK receptors, as well as CKK release, exhibits considerable plasticity after nerve injury and inflammation, conditions known to be associated with chronic pain. Such altered CCK release coupled in some situation with changes in CCK receptor levels may underlie the clinical phenomenon of varying opioid sensitivity in different clinical pain conditions. In particular, neuropathic pain after injury to the peripheral and central nervous system does not respond well to opioids, which is likely to be caused by increased activity in the endogenous CCK system. CCK receptor antagonists may thus be useful as analgesics in combination with opioids to treat neuropathic pain.

Topics: Analgesia; Animals; beta-Endorphin; Cholecystokinin; Chronic Disease; Humans; Inflammation; Morphine; Pain; Rats; Receptors, Cholecystokinin; Spinal Cord Injuries

Topics: Adult; Aged; beta-Endorphin; Chronic Disease; Depressive Disorder; Dexamethasone; Endorphins; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Middle Aged; Pain; Pituitary Hormones, Anterior; Pituitary-Adrenal System

To explore the clinical efficacy of acupoint catgut embedding therapy on chronic pelvic cavity pain syndrome differentiated as kidney deficiency and stagnation of damp heat, and explore the impacts on plasma P substance (SP), plasma beta-endorphin (β-EP).. One hundred and eighty cases were randomly divided into a catgut embedding group (90 cases) and a western medication group (90 cases). In the western medication group, tamsulosin capsules 0. 2 mg were prescribed for oral administration, once a day; indometacin sustained release tablets, 25 mg, three times a day. Totally, the oral administration for 8 weeks was required. In the catgut embedding group, the acupoint catgut embedding therapy was applied to Qugu (CV 2), Shenshu (BL 23), Zhibian (BL 54), Huiyin (CV 1) and Sanyinjiao (SP 6), once every two weeks; the treatment of 4 weeks made one session, and two sessions were required. Before and after treatment, TCM symptom score, NIH-CPSI (the National Institute of Health Chronic Prostatitis Symptom Index) score, lecithin body numbers in prostatic fluid, score in SAS (self-rating anxiety scale), score in SDS (self-rating depression scale), the levels of SP and β-EP, etc. were observed in the two groups, and the clinical efficacy was assessed in the two groups.. (1) Ten cases were dropped in either group. The total effective rate was 91. 25% (73/80) in the catgut embedding group, higher than 78. 75% (63/80) in the western medication group (P<0. 05). (2) After treatment, TCM symptom score, total score in NIH-CPSI, pain score and the scores in SAS and SDS were all reduced as compared with those before treatment in the two groups (all P<0. 05). After treatment, TCM symptom score, total score and pain score in NIH-CPSI, and the scores in SAS and SDS in the catgut embedding group were both lower than those in the western medication group (all P<0. 05). (3) After treatment, the lecithin body numbers were both increased as compared with those before treatment in the two groups (both P<0. 05), and the result in the catgut embedding group was higher than that in the western medication group (P<0. 05). (4)After treatment, the SP level was lower than that before treatment in the two groups (both P<0. 05); the level of p-EP was increased as compared with that before treatment (both P<0. 05). The SP level in the catgut embedding group was lower than that in the western medication group (P<0. 05); the level of β-EP was higher than that in the western medication group (P<0. 05).. The acupoint catgut embedding therapy apparently relieves the clinical symptoms of chronic pelvic cavity pain syndrome differentiated as kidney deficiency and stagnation of damp heat as well as the condition of anxiety and depression, increases lecithin body numbers in prostatic fluid and β-EP level and reduces SP level.

Topics: Acupuncture Points; Acupuncture Therapy; Adolescent; Adult; beta-Endorphin; Catgut; Chronic Disease; Humans; Male; Pelvic Pain; Prostatic Diseases; Young Adult

Previously it was shown that a brief yoga-based lifestyle intervention was efficacious in reducing oxidative stress and risk of chronic diseases even in a short duration. The objective of this study was to assess the efficacy of this intervention in reducing stress and inflammation in patients with chronic inflammatory diseases.. This study reports preliminary results from a nonrandomized prospective ongoing study with pre-post design.. The study was conducted at the Integral Health Clinic, an outpatient facility conducting these yoga-based lifestyle intervention programs for prevention and management of chronic diseases.. Patients with chronic inflammatory diseases and overweight/obese subjects were included while physically challenged, and those on other interventions were excluded from the study.. A pretested intervention program included asanas (postures), pranayama (breathing exercises), stress management, group discussions, lectures, and individualized advice.. There was a reduction in stress (plasma cortisol and β-endorphin) and inflammation (interleukin [IL]-6 and tumor necrosis factor [TNF]-α) at day 0 versus day 10.. Eighty-six (86) patients (44 female, 42 male, 40.07 ± 13.91 years) attended this program. Overall, the mean level of cortisol decreased from baseline to day 10 (149.95 ± 46.07, 129.07 ± 33.30 ng/mL; p=0.001) while β-endorphins increased from baseline to day 10 (3.53 ± 0.88, 4.06 ± 0.79 ng/mL; p=0.024). Also, there was reduction from baseline to day 10 in mean levels of IL-6 (2.16 ± 0.42, 1.94 ± 0.10 pg/mL, p=0.036) and TNF-α (2.85 ± 0.59, 1.95 ± 0.32 pg/mL, p=0.002).. This brief yoga-based lifestyle intervention reduced the markers of stress and inflammation as early as 10 days in patients with chronic diseases; however, complete results of this study will confirm whether this program has utility as complementary and alternative therapy.

Topics: Adult; beta-Endorphin; Breathing Exercises; Chronic Disease; Counseling; Female; Group Processes; Health Education; Humans; Hydrocortisone; Inflammation; Interleukin-6; Life Style; Male; Meditation; Middle Aged; Obesity; Relaxation Therapy; Stress, Psychological; Treatment Outcome; Tumor Necrosis Factor-alpha; Yoga

To investigate the clinical effect of electroacupuncture (EA) for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).. We recruited 63 participants meeting the U.S. National Institutes of Health (NIH) consensus criteria for CP/CPPS. After the inclusion/exclusion criteria were applied, 39 men were randomized to 3 treatment groups: group 1, advice and exercise plus 12 sessions of EA; group 2, advice and exercise plus 12 sessions of sham EA (SEA); and group 3, advice and exercise alone (A&E) for 6 weeks. A total of 6 acupuncture points were used to stimulate the sacral nerve and release the piriformis muscle using an electrical pulse generator. Symptoms related to CP/CPPS were assessed using the NIH-Chronic Prostatitis Symptom Index (NIH-CPSI). Prostaglandin E(2) and beta-endorphin levels in postmassage urine samples were measured using an enzyme-linked immunosorbent assay.. At 6 weeks, the NIH-CPSI total score had decreased significantly in the EA group compared with the SEA and A&E groups (P < .001). On a subscale analysis of the NIH-CPSI, the EA group showed significant decreases in pain-related symptoms compared with the SEA and A&E groups (P < .01). All 12 EA participants experienced at least a 6-point decrease in the NIH-CPSI total score compared with 2 of 12 SEA participants (16.7%) and 3 of 12 A&E participants (25.0%; P < .0001). The mean prostaglandin E(2) level in the postmassage urine samples had significantly decreased in the EA group (P = .023). In contrast, it had increased in the other 2 groups.. In a 3-arm randomized trial investigating the clinical effects of EA on CP/CPPS, EA therapy proved to have independent therapeutic effects, particularly for pain relief superior to SEA or A&E therapy.

Topics: Adult; beta-Endorphin; Biomarkers; Chronic Disease; Dinoprostone; Electroacupuncture; Enzyme-Linked Immunosorbent Assay; Exercise; Follow-Up Studies; Humans; Male; Middle Aged; Pain Measurement; Patient Education as Topic; Patient Satisfaction; Pelvic Pain; Probability; Prostatitis; Reference Values; Risk Assessment; Statistics, Nonparametric; Syndrome; Treatment Outcome

The anger management styles of anger-in (inhibition) and anger-out (direct expression) are positively associated with pain responsiveness. Opioid blockade studies suggest that hyperalgesic effects of trait anger-out, but not those of trait anger-in, are mediated in part by opioid analgesic system dysfunction. The current study tested the opioid dysfunction hypothesis of anger-out using an alternative index of opioid function: pain-induced changes in plasma endogenous opioids. Plasma beta-endorphin (BE) was assessed at rest and again following exposure to three laboratory acute pain tasks (finger pressure, ischemic, and thermal) in 14 healthy controls and 13 chronic low back pain (LBP) subjects. As expected, acute pain ratings correlated positively with measures of anger-in (both groups) and anger-out (LBP group; p's<.05). Greater pain-induced increases in BE were associated with significantly lower pain ratings in both groups (p's<.05). Hierarchical multiple regression indicated that greater anger-out significantly predicted smaller pain-induced BE increases (p<.05). Subject type did not moderate this association (p>.10). Anger-in did not display significant main or interaction effects on pain-induced BE changes (p's>.10). The significant association between anger-out and BE release partially mediated the hyperalgesic effects of anger-out on pain unpleasantness, and was not attenuated by statistical control of general negative affect. This suggests unique associations with expressive anger regulation. Elevated trait anger-out therefore appears to be associated with opioid analgesic system dysfunction, whether it is indexed by responses to opioid blockade or by examining circulating endogenous opioid levels. Possible "statextrait" interactions on these anger-related opioid system differences are discussed.

Topics: Acute Disease; Adrenergic alpha-Antagonists; Adult; Anger; beta-Endorphin; Chronic Disease; Female; Hot Temperature; Humans; Ischemia; Low Back Pain; Male; Pain Measurement; Pain Threshold; Pressure; Yohimbine

Cardiomyocytes produce opioid peptides and receptors. beta-Endorphin is increased in the plasma of patients with congestive heart failure (CHF). We evaluated whether an intravenous infusion of beta-endorphin exerted any effect on cardiovascular function and on the neurohormonal milieu in patients with mild to moderate CHF.. According to a double-blind, placebo-controlled design, 10 patients (5 men, age 46.9 +/- 8.2 years [mean +/- SD]) with CHF and New York Heart Association functional class II to III received, in random order, 1-hour intravenous infusion of beta-endorphin (500 microg/h) and, on a separate occasion, received placebo and underwent echocardiographic and laboratory measurements at baseline and during infusions.. beta-Endorphin significantly increased left ventricular ejection fraction (LVEF) (P =.0001) and stroke volume (P =.0001), and reduced systemic vascular resistance (P =.031) in patients with CHF. These changes were paralleled by a significant increase in plasma levels of glucagon (P =.0001), GH (P =.0001), and IGF-1 (P =.0001), and a significant decrease in plasma levels of endothelin (P =.0001) and catecholamines (P =.01). No hemodynamic and neurohormonal changes were observed during the placebo study in any patient.. We conclude that a short-term, high dose infusion of beta-endorphin improves LVEF, reduces systemic vascular resistance, blunts the neurohormonal activation, and stimulates the GH/IGF-1 axis in patients with mild to moderate CHF.

Topics: Adult; beta-Endorphin; Cardiomyopathy, Dilated; Catecholamines; Chronic Disease; Echocardiography; Exercise Test; Exercise Tolerance; Female; Hemodynamics; Humans; Infusions, Intravenous; Male; Middle Aged; Stroke Volume

Stimulation of the antinociceptive system by noninvasive electrical current from electrodes placed on the head is a renewed method of pain relief.. We conducted a randomized, double-blind, placebo-controlled study on 20 chronic back pain patients. They were treated with either transcranial electrostimulation (TCES) or an active placebo device. Pain level and serum beta-endorphin levels were measured before and after treatment.. beta-Endorphin level increased in seven of the ten patients from the treatment group and did not change in eight of ten patients from control group (P = 0.057 between groups). Pain level decreased in eight treated patients and seven control patients (significant decrease for each group, no significant difference between groups).. Transcranial electrostimulation is a nonpharmacologic method of pain relief accompanied or mediated by beta-endorphin release. The comparable degree of the initial clinical response emphasizes the powerful placebo effect on reported pain not mediated by endorphin release. This preliminary study shows that noninvasive electrical stimulation is a safe treatment with a positive effect on beta-endorphin blood levels.

Topics: Adult; Aged; beta-Endorphin; Chronic Disease; Double-Blind Method; Electric Stimulation Therapy; Female; Humans; Low Back Pain; Male; Middle Aged; Neck Pain; Pain Measurement; Placebo Effect; Treatment Outcome

The purpose of the present study was to investigate whether the floating form of the restricted environmental stimulation technique (REST) may be applied within the field of pain relief. Flotation-REST consists of a procedure whereby an individual is immersed in a tank filled with water of an extremely high salt concentration. Thirty-seven patients (14 men and 23 women) suffering from chronic pain consisting of aching muscles in the neck and back area participated in the study. They were randomly assigned to either a control group (17 participants) or an experimental group (20 participants). The experimental group received nine opportunities to use the flotation-REST technique in the water tank over a three-week period. The results indicated that the most severe perceived pain intensity was significantly reduced, whereas low perceived pain intensity was not influenced by the floating technique. Further, the results indicated that circulating levels of the noradrenaline metabolite 3-methoxy-4-hydroxyphenylethyleneglycol were reduced significantly in the experimental group but not in the control group following treatment, whereas endorphin levels were not affected by flotation. Flotation-REST treatment also elevated the participants' optimism and reduced the degree of anxiety or depression; at nighttime, patients who underwent flotation fell asleep more easily. The present findings describe possible changes, for the better, in patients presenting with chronic pain complaints.

Topics: Adult; Anxiety; beta-Endorphin; Chronic Disease; Depression; Female; Headache; Humans; Male; Methoxyhydroxyphenylglycol; Muscle Contraction; Pain; Pain Management; Personality; Psychophysiologic Disorders; Relaxation Therapy; Reproducibility of Results; Sleep

In a canine model of congestive heart failure beta endorphin concentrations were high and opioid receptor antagonists exerted beneficial haemodynamic effects. In humans previous studies have suggested that opioid peptides may modify the perception of breathlessness and fatigue in heart failure.. Plasma concentrations of beta endorphin were measured in patients with acute and chronic heart failure and cardiogenic shock. A subgroup of eight patients with New York Heart Association (NYHA) class III-IV heart failure was assessed for acute haemodynamic effects of naloxone, an opioid receptor antagonist. A separate group of 10 patients with class II-III heart failure, was randomised to a double blind placebo controlled study of the effects of intravenous naloxone on cardiopulmonary exercise performance.. Plasma concentrations of beta endorphin were usually normal in patients with chronic heart failure and did not correlate with severity as assessed by NYHA class. In 29% of patients with acute heart failure and 71% of those with cardiogenic shock beta endorphin concentrations were high. The median concentration in the cardiogenic shock group was significantly higher than in either of the two heart failure groups and there was some evidence of a relation between beta endorphin concentrations and survival. At the doses tested, naloxone was unable to modify systemic haemodynamics, exercise performance, or symptoms in patients with chronic congestive heart failure.. Circulating concentrations of beta endorphin are usually normal in patients with chronic congestive heart failure. Inhibition of the endogenous opioid system is unlikely to have therapeutic potential in heart failure.

Topics: Acute Disease; Adult; Aged; beta-Endorphin; Chronic Disease; Double-Blind Method; Exercise Test; Female; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Naloxone; Shock, Cardiogenic; Stroke Volume; Ventricular Function, Left

Nicotine is known to release neuroendocrine substances which may subsequently reinforce smoking behavior by improving mood states. The purpose of this study was to examine changes in plasma beta-endorphin and mood states during periods of chronic smoking, abstinence from smoking, and abstinence while chewing nicotine gum. A modified A-B-A-C design was used. Normal male volunteers were randomly assigned to an experimental or control group. Over a 12-day protocol, experimental subjects smoked ad libitum for 2 days, were abstinent for 4 days, resumed smoking for 2 days, and then chewed nicotine gum for the final 4 days. Control subjects smoked ad libitum throughout the entire protocol. Results indicated that changes in plasma beta-endorphin levels were not related to changes in the four smoking conditions. Plasma nicotine and mood states were related, such that dysphoric moods increased during abstinence from smoking in comparison to the control group. To investigate further the relationships between nicotine, beta-endorphin and reinforcement for smoking, it may be necessary to characterize endogenous opioid peptide release in the central nervous system during smoking.

Topics: Adult; Affect; beta-Endorphin; Chronic Disease; Humans; Male; Nicotine; Smoking; Smoking Cessation; Substance Withdrawal Syndrome; Surveys and Questionnaires

Sixty patients with chronic pain of the low back or cervical spine concomitant with clinical depression were studied in a 6-week, randomized, double-blind comparison of doxepin and placebo. Significant improvements in the doxepin-treated group compared to placebo or to baseline values were seen on Hamilton depression scores, Global Assessment Scale scores, pain severity, percent of time pain felt, and effect of pain on activity, sleep, and muscle tension. Some improvements were observed after 1 week of treatment; the most improvement occurred at 6 weeks, when the mean doxepin dosage was approximately 200 mg/day and plasma doxepin and nordoxepin averaged 80 ng/ml. No significant harmful effects were observed. Neither plasma beta-endorphin nor enkephalin-like activity demonstrated significant differences from baseline. These data indicate that doxepin is a valuable treatment for patients with chronic pain and depression.

Topics: beta-Endorphin; Chronic Disease; Clinical Trials as Topic; Depressive Disorder; Double-Blind Method; Doxepin; Endorphins; Enkephalins; Female; Humans; Male; Middle Aged; Pain; Placebos; Psychiatric Status Rating Scales; Random Allocation; Time Factors

Doxepin and desipramine at final doses of 188 and 173 mg/day, respectively, were compared in 36 volunteers with major affective or dysthymic disorder and chronic back pain. Both drugs produced significant decreases in depression, with an overall response rate of 70%; no significant difference was seen between groups. Pain ratings also decreased significantly in both groups (overall response rate = 50%); pain severity showed a better response to doxepin than to desipramine. While baseline pain, depression, and anxiety were correlated, treatment changes in these measures did not correlate. CSF beta-endorphin levels did not change with treatment. The usefulness of an antidepressant with anxiolytic properties, such as doxepin, is discussed.

Topics: Adult; Anxiety Disorders; Back Pain; beta-Endorphin; Chronic Disease; Clinical Trials as Topic; Depressive Disorder; Desipramine; Doxepin; Endorphins; Female; Helplessness, Learned; Humans; Male; Personality Inventory; Placebos; Psychiatric Status Rating Scales

Thirty patients with chronic low back or cervical pain combined with clinical depression were studied in a six-week, randomized, double-blind comparison of doxepin and placebo. Dependent variables included Hamilton Depression Scores, the Clinical Global Assessment Scale, and Profile of Mood States (POMS), and subjective ratings (visual analogue scales) of pain severity, percent of time pain felt, and effect of pain on activity, muscle tension, sleep, mood, and analgesic drug consumption. Plasma levels of doxepin, desmethyldoxepin, beta-endorphin, and enkephalin-like activity were also measured. Significant improvements in the doxepin-treated group compared to the placebo group were seen in Hamilton scores, Global Assessment Scale, Profile of Mood States, percent of time pain felt, and effect of pain on sleep, muscle tension, and mood. Some improvement was observed after 1 week, although most improvement occurred at 6 weeks, when the mean doxepin dose was 2.5 mg/kg and plasma doxepin and desmethyldoxepin averaged 70 ng/ml. Nonspecific enkephalin-like activity (but not beta-endorphins) increased for the treatment group and decreased for the placebo group. The efficacy of doxepin compared with that of placebo was thus documented in several depressive and pain parameters, indicating that doxepin is a valuable treatment for patients with chronic pain and depression.

Topics: Adult; Aged; beta-Endorphin; Chronic Disease; Depression; Double-Blind Method; Doxepin; Endorphins; Enkephalins; Female; Humans; Male; Middle Aged; Pain; Placebos; Random Allocation; Sensory Thresholds; Sleep

 This study investigated the sex differences of the inflammatory mediator level at the time of itch onset in patients with chronic venous disease (CVD). Twenty-seven CVD patients (nineteen women, eight men) and nine healthy controls (five women, four men) participated. CVD-associated itching was observed in both men and women. Before sclerotherapy, both sexes had elevations in several itch-related mediators. Among these, women had significantly higher tryptase, whereas men had significantly higher β-endorphin and adrenocorticotropic hormone. After sclerotherapy, all levels normalized in both sexes. In this study, itching was increased tryptase in women and increased adrenocorticotropic hormone and β-endorphin in men.

Topics: Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; Chronic Disease; Female; Humans; Inflammation Mediators; Male; Middle Aged; Pruritus; Sclerotherapy; Sex Characteristics; Tryptases; Vascular Diseases

Psychological stress accompanies chronic inflammatory diseases such as IBD, and stress hormones can exacerbate pain signalling. In contrast, the endogenous opioid system has an important analgesic action during chronic inflammation. This study examined the interaction of these pathways.. Mouse nociceptive dorsal root ganglia (DRG) neurons were incubated with supernatants from segments of inflamed colon collected from patients with chronic UC and mice with dextran sodium sulfate (cDSS)-induced chronic colitis. Stress effects were studied by adding stress hormones (epinephrine and corticosterone) to dissociated neurons or by exposing cDSS mice to water avoidance stress. Changes in excitability of colonic DRG nociceptors were measured using patch clamp and Ca. Supernatants from patients with chronic UC and from colons of mice with chronic colitis caused a naloxone-sensitive inhibition of neuronal excitability and capsaicin-evoked Ca. Stress hormones block the inhibitory actions of endogenous opioids and can change the effect of opioid signalling in DRG neurons to excitation. Targeting these pathways may prevent heavy opioid use in IBD.

Topics: Adult; Aged; Animals; beta-Endorphin; Biopsy; Chronic Disease; Colitis; Colon; Cytokines; Ganglia, Spinal; Humans; Mice; Mice, Inbred C57BL; Middle Aged; Naloxone; Nociceptors; Patch-Clamp Techniques; Signal Transduction; Stress, Psychological

Biomarker for prediction of development of low back pain, and disease progression in chronic conditions are virtually non-existent. In the present study, we examined evidence of inflammation in the peripheral blood and demonstrated significant changes in neuroinflammation markers in subjects with chronic low back pain in comparison with control subjects. The present study was performed using peripheral blood from subjects with chronic low back pain and age-matched control subjects. Western blotting, real-time RT-PCR, cell culture and in vitro assays were incorporated to perform the current study. We obtained evidence that the balance between proinflammatory and anti-inflammatory cytokines is misaligned, with decrease in interleukin-10 (IL-10) expression and increase in interleukin-6 (IL-6) expression. Furthermore, we demonstrated increase in CD16 monocyte expression. Cells were cultured under differential conditions to generate M1/M2 macrophages. In the macrophages, opioid secretory capacity was shown to be diminished. Finally, Dragon (repulsive guidance molecule b, RGMb) expression was shown diminished in M1 macrophages, which serves as a key transcriptional inhibitor of IL-6 expression. These biochemical and cellular alterations in chronic low back pain can serve as potential biomarkers for assessing disease initiation, intensity and progression.

Topics: Aged; beta-Endorphin; Biomarkers; Case-Control Studies; Cell Adhesion Molecules, Neuronal; Cell Differentiation; Chronic Disease; Female; Humans; Interleukin-10; Interleukin-6; Low Back Pain; Macrophages; Male; Middle Aged; Monocytes; Primary Cell Culture; Th1-Th2 Balance; Transcription, Genetic

In peripheral tissue, several substances influence pain and pain modulation. Exercise has been found to decrease pain and improve function for chronic pain conditions, but how and why exercise produces beneficial effects remains unclear. This study investigates whether aspects of pain and concentrations of substances with algesic, analgesic and metabolic functions differ between women with chronic neck shoulder pain (CNSP) and healthy women (CON) and whether changes are found after an exercise intervention for CNSP.. Forty-one women with CNSP and 24 CON subjects were included. The participants attended two microdialysis sessions with 4-6 months between the experiments. During this period, the CNSP subjects underwent an exercise intervention. Expression levels of substance P, beta-endorphin, cortisol, glutamate, lactate and pyruvate as well as pain intensity and pressure pain thresholds were analysed.. At baseline, higher concentrations of glutamate and beta-endorphin and lower concentrations of cortisol in CNSP than CON were found. After exercise, decreased levels of substance P and possibly of glutamate, increased levels of beta-endorphin and cortisol as well as decreased pain intensity and increased pain pressure thresholds were found for CNSP.. The findings at baseline indicated algesic and analgesic alterations in the painful trapezius muscles. The findings for CNSP after the exercise intervention, with changes in peripheral substances and decreased pain intensity and sensitivity, could reflect a long-term physiological effect of the exercise.

Topics: Adult; beta-Endorphin; Chronic Disease; Exercise Therapy; Female; Glutamic Acid; Humans; Hydrocortisone; Lactic Acid; Microdialysis; Middle Aged; Neck Pain; Pain Measurement; Pain Threshold; Pyruvic Acid; Shoulder Pain; Substance P; Superficial Back Muscles; Young Adult

To investigate the relationship of the common Traditional Chinese Medicine (TCM) syndrome pattern of chronic pelvic pain syndrome (CPPS) with the contents of substance p and beta endorphin in the plasma, and provide reference data for the clinical diagnosis, differentiation and treatment of CPPS by TCM.. We observed 98 cases of CPPS, which were classified into a lower-part damp-heat invasion group (group A, n = 32), a blood stasis-induced collateral obstruction group (group B, n = 34), and a damp-heat stagnation group (group C, n = 32) according to the TCM syndrome differentiation. Another 35 normal healthy young men were enrolled as controls. We measured the contents of substance p and beta endorphin in the plasma by immunoradiometry and ELISA, and analyzed their relationship with the TCM syndrome pattern.. The contents of plasma substance p were significantly higher in groups A ([1135.76 +/- 166.45] pg/ml), B ([1 337.84 +/- 170.81] pg/ml), and C ([1 210.01 +/- 162.27] pg/ml) than in the control ([574.99 +/- 113.09] pg/ml) (all P < 0.01), while the contents of plasma beta endorphin in groups A ([212.70 +/- 29.49] pg/ml), B ([157.99 +/- 24.01] pg/ml), and C ([180.81 +/- 20.20] pg/ml) were remarkably lower than that in the control ([274.73 +/- 27.64] pg/ml) (all P < 0.01).. In the plasma of CPPS patients, the content of substance p is significantly elevated and that of beta endorphin markedly reduced, which suggests that they may be involved in the inflammatory reaction of CPPS. The levels of plasma substance p and beta endorphin can be used as valuable reference for the TCM classification of chronic prostatitis.

Topics: beta-Endorphin; Case-Control Studies; Chronic Disease; Humans; Male; Medicine, Chinese Traditional; Pelvic Pain; Prostatitis; Substance P; Syndrome

Endogenous opioids are implicated in pain-regulation in chronic inflammatory bowel disease (IBD). We sought to examine whether endogenous opioids suppress the excitability of colonic nociceptive dorsal root ganglia (DRG) neurons during chronic IBD, and if so, whether modulation of underlying voltage-gated K(+) currents was involved.. The effects of chronic dextran sulfate sodium (DSS) colitis on afferent signaling in mice was studied using patch clamp recordings. Colonic DRG neurons were identified using Fast Blue retrograde labeling and recordings obtained from small DRG neurons (<40 pF).. In current-clamp recordings, the rheobase of neurons was increased 47% (P < 0.01) and action potential discharge at twice rheobase decreased 23% (P < 0.05) following incubation in colonic supernatants from chronic DSS mice. β-endorphin increased 14-fold, and tissue opioid immunoreactivity and expression in CD4+ cells observed by flow cytometry increased in chronic DSS colons. Incubation of naïve neurons in the μ-opioid receptor agonist D-Ala(2), N- MePhe(4), Gly-ol (DAMGO) (10 nM) partially recapitulated the effects of supernatants from DSS mice on rheobase. Supernatant effects were blocked by the μ-opioid receptor antagonist naloxone. In voltage clamp, chronic DSS supernatants and DAMGO increased I(A) K(+) currents.. The release of endogenous opioids during chronic inflammation in mice suppresses the excitability of nociceptive DRG neurons. Targeting immune cells may provide a novel means of modulating IBD pain.

Topics: Action Potentials; Animals; beta-Endorphin; Cell Separation; Chronic Disease; Colon; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Ganglia, Spinal; Immunohistochemistry; Inflammatory Bowel Diseases; Mice; Mice, Inbred C57BL; Patch-Clamp Techniques

To explore the mechanism of electroacupuncture (EA)-induced cumulative analgesic effects on chronic pain in rats with or without ovariectomy (OVX).. A total of 110 female Wistar rats were randomized into normal control (n=10), chronic constrictive injury (CCI, n=10), CCI+EA (n=30), OVX+CCI (n=30), and OVX+CCI+EA (n=30) groups. Each of the latter 3 groups was further divided into 2 days (2 d), 2 weeks (2 W) and 3 weeks (3 W) subgroups, respectively (n=10 in each subgroup). The CCI pain model was established by ligature of the right sciatic nerve, and the memory impairment model duplicated by OVX. The paw withdrawal latency (PWL, pain threshold) of the bilateral footplates was detected by radiant heat irradiation, and the bilateral difference in PWL (PWLD) was used to evaluate changes in the pain reaction. Morris water maze test was conducted for evaluating the rats' learning-memory ability. EA was applied to bilateral Zusanli (ST36) and Yanglingquan (GB34) for 2 d, 2 W and 3 W, respectively. Pituitary and hypothalamic beta-endorphin (EP) and adrenocorticotrophic hormone (ACTH) contents were detected by immunoradioassay.. Compared with the CCI group, PWLD of the CCI+EA-3 W group decreased significantly (P<0.05). Compared with the OVX+CCI group, PWLD of the OVX+CCI+EA-3 W group was lowered considerably (P<0.05), but the value was markedly higher than its basal value and those of the normal control and CCI+EA groups (P<0.05). In comparison with the sham-OVX group, the escape latency, swimming distance (SD) in the target quadrant and total SD were increased remarkably in the OVX group (P<0.05), while the number of target platform crossings was decreased significantly (P<0.05), suggesting an impairment of the OVX rats' learning-memory ability. In simple CCI rats, both beta-EP and ACTH contents of the pituitary increased markedly (P<0.05), and those of the hypothalamus decreased obviously compared to the normal control group (P<0.05). After EA, pituitary and hypothalamic ACTH levels were significantly lowered at 2 d and hypothalamic ACTH and beta-EP contents increased obviously at 3 W in comparison with the CCI group (P<0.05). In OVX+CCI rats, following EA, pituitary beta-EP contents at 2 d, 2 W and 3 W, and hypothalamic beta-EP and ACTH contents at 2 W and hypothalamic ACTH levels at 3 W increased significantly (P<0.05), but hypothalamic beta-EP level at 3W decreased markedly (P<0.05). The effects of repeated EA in lowering pituitary ACTH and raising hypothalamic beta-EP and ACTH levels disappeared after OVX+CCI.. Repeated EA has a cumulative analgesic effect, which is closely associated with its effects in regulating pituitary and hypothalamic beta-EP and ACTH levels. OVX may weaken the analgesic effect of EA by affecting hypothalamic-pituitary axis activity.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; Chronic Disease; Electroacupuncture; Female; Hypothalamus; Memory; Ovariectomy; Pain Management; Pituitary Gland; Rats; Rats, Wistar

Lumbar puncture (LP) is an attractive route to deliver drugs to the nervous system because it is a safe bedside procedure. Its use for gene therapy has been complicated by poor vector performance and failure to target neurons. Here we report highly effective gene transfer to the primary sensory neurons of the dorsal root ganglia (DRGs) with self-complementary recombinant adeno-associated virus serotype 8 (sc-rAAV8) modeling an LP. Transgene expression was selective for these neurons outlining their cell bodies in the DRGs and their axons projecting into the spinal cord. Immunohistochemical studies demonstrated transduction of cells positive for the nociceptive neuron marker vanilloid receptor subtype 1, the small peptidergic neuron markers substance P and calcitonin gene-related peptide, and the nonpeptidergic neuron marker griffonia simplicifolia isolectin B4. We tested the efficacy of the approach in a rat model of chronic neuropathic pain. A single administration of sc-rAAV8 expressing the analgesic gene prepro-beta-endorphin (ppbetaEP) led to significant (P < 0.0001) reversal of mechanical allodynia for >/=3 months. The antiallodynic effect could be reversed by the mu-opioid antagonist naloxone 4 months after gene transfer (P < 0.001). Testing of an alternative nonopioid analgesic gene, IL-10, alone or in combination with ppbetaEP was equally effective (P < 0.0001). All aspects of the procedure, such as the use of an atraumatic injection technique, isotonic diluent, a low-infusion pressure, and a small injection volume, are consistent with clinical practice of intrathecal drug use. Therefore, gene transfer by LP may be suitable for developing gene therapy-based treatments for chronic pain.

Topics: Animals; beta-Endorphin; Chronic Disease; Dependovirus; Disease Models, Animal; Genetic Therapy; Genetic Vectors; Immunohistochemistry; Kinetics; Male; Neurons, Afferent; Pain; Pain Management; Peripheral Nervous System Diseases; Protein Precursors; Rats; Rats, Sprague-Dawley; Receptors, Opioid; Spinal Puncture

Even though inflammation is a traditional tool for the induction of hyperalgesia in many tissues, recent observations suggest that not all inflammatory processes produce this change. Tolerance to colorectal distension (CRD) is reduced in patients with acute ulcerative colitis but is increased in patients with chronic inflammatory bowel disease. This suggests that the nature of the inflammatory infiltrate influences visceral perception.. To test this hypothesis by assessing responses to CRD in mice with mild, acute or chronic colitis.. CRD responses were measured in mice with mild non-specific colitis, and dextran sodium sulphate (DSS)-induced acute and chronic colitis. Responses were compared with tissue infiltrate and damage, interleukin (IL)1beta and myeloperoxidase (MPO) activity and substance P, beta-endorphin and micro opioid receptor (MOR) expression.. Mild and acute colitis were associated with increased responsiveness to CRD. In contrast, CRD responses were not increased in mice with chronic colitis and this difference was not due to altered colonic wall compliance. MPO and IL1beta levels were greater in acute than in chronic colitis. Larger increases in tissue substance P were seen in acute than in chronic DSS, whereas CD4 T cells, beta-endorphin and MOR expression were evident only in chronic colitis. An inverse correlation was seen between substance P and MOR in these tissues.. Acute colitis increased responsiveness to CRD and is accompanied by an acute inflammatory infiltrate and increased tissue substance P. Chronic DSS is accompanied by an increase in beta-endorphin and MOR expression, and CD4 T cells, but no change in compliance or CRD responses. We conclude that acute inflammation generates hyperalgesia, whereas chronic inflammation involves infiltration by lymphocytes accompanied by MOR and beta-endorphin up regulation, and this provides an antinociceptive input that restores normal visceral perception.

Topics: Acute Disease; Animals; beta-Endorphin; CD4-Positive T-Lymphocytes; Chronic Disease; Colitis; Colon; Compliance; Interleukin-1beta; Male; Mice; Mice, Inbred BALB C; Neuropeptides; Pain; Pain Threshold; Physical Stimulation; Receptors, Opioid, mu; Substance P

Acute nicotine administration has been shown to activate the hypothalamic-pituitary-adrenal (HPA) axis and stimulate secretion of adrenocorticotrophic hormone (ACTH), corticosterone/cortisol and beta-endorphin (beta-END) in both rodents and humans, raising the possibility that activation of the HPA axis by nicotine may mediate some of the effects of nicotine. Since stress can increase the risk of drug use and abuse, we hypothesized that repeated stress would increase the ability of nicotine to stimulate the secretion of HPA hormones. To test our hypothesis, mice were exposed to repeated stress (swimming in 15 degrees C water for 3 min/day for 5 days) and killed 15 min after injection of saline or nicotine (0.1 mg/kg, s.c.). Repeated exposure to stress increased the ability of nicotine to stimulate plasma ACTH (p<0.05) and beta-END (p<0.05), but not corticosterone secretion. In contrast, repeated exposure to stress increased the post-saline injection levels of corticosterone (p<0.05), but not ACTH and beta-END. The present results suggest that chronic stress leads to an enhanced sensitivity of some components of the HPA axis to a subsequent nicotine challenge.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; Chronic Disease; Corticosterone; Disease Models, Animal; Hypothalamo-Hypophyseal System; Male; Mice; Mice, Inbred C57BL; Nicotine; Nicotinic Agonists; Pituitary-Adrenal System; Stress, Psychological; Tobacco Use Disorder

We and others have demonstrated that impaired arterial baroreceptor reflex (ABR) function is one of the major causes of hypertension-associated end organ damage. The goal of this study was to clarify the potential neuro-humoral mechanisms responsible for impaired ABR-induced end organ damage. The sino-aortic denervated (SAD) rat was used as an animal model of ABR dysfunction. One-week SAD rats were characterized by hypertension, tachycardia, increased norepinephrine content, and decreased beta-endorphin and leu-enkephalin content in hypothalamus and medulla oblongata, and increased plasma levels of arginine-vasopressin. In 18-week SAD rats, the 24-hour average arterial pressure, heart rate, beta-endorphin, and leu-enkephalin content in hypothalamus and medulla oblongata and plasma levels of arginine-vasopressin and angiotensin II were not different from those measured in ABR-intact rats. However, blood pressure variability and angiotensin II content in kidney and left ventricle increased. When exposed to chronic stress, exaggerated changes in arterial pressure, blood pressure variability, the levels of central norepinephrine, beta-endorphin and leu-enkephalin, plasma arginine-vasopressin and angiotensin II, and tissue angiotensin II were found in 18-week SAD rats. These data indicate that a long-term impairment of ABR leads to chronic activation of central noradrenergic neurons and tissue renin-angiotensin system, and that stress induces exaggerated responses of neuro-humoral factors and hemodynamics in SAD rats. Thus, if the present results hold true for humans, one can expect abnormal neurotransmitter/neuromodulator responses to environmental insults in patients with impaired ABR function.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Baroreflex; beta-Endorphin; Blood Pressure; Brain; Chronic Disease; Denervation; Enkephalin, Leucine; Heart Rate; Hypertension; Male; Norepinephrine; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Sinoatrial Node

There is evidence that neuropeptides, especially the opiate receptor agonists, are involved in wound healing. We have previously observed that beta-endorphin, the endogenous ligand for the mu-opiate receptor, stimulates the expression of cytokeratin 16 in a dose-dependent manner in human skin organ cultures. Cytokeratin 16 is expressed in hyperproliferative epidermis such as psoriasis and wound healing. Therefore we were interested to study whether epidermal mu-opiate receptor expression is changed at the wound margins in acute and chronic wounds. Using classical and confocal microscopy, we were able to compare the expression level of mu-opiate receptors and the influence of beta-endorphin on transforming growth factor beta type II receptor in organ culture. Our results show indeed a significantly decreased expression of mu-opiate receptors on keratinocytes close to the wound margin of chronic wounds compared to acute wounds. Additionally beta-endorphin upregulates the expression of transforming growth factor beta type II receptor in human skin organ cultures. These results suggest a crucial role of opioid peptides not only in pain control but also in wound healing. Opioid peptides have already been used in animal models in treatment of wounds; they induce fibroblast proliferation and growth of capillaries, and accelerate the maturation of granulation tissue and the epithelization of the defect. Furthermore opioid peptides may fine-tune pain and the inflammatory response while healing takes place. This new knowledge could potentially be used to design new locally applied drugs to improve the healing of painful chronic wounds.

Topics: Acute Disease; beta-Endorphin; Chronic Disease; Dose-Response Relationship, Drug; Gene Expression Regulation; Humans; Keratins; Organ Culture Techniques; Protein Serine-Threonine Kinases; Receptor, Transforming Growth Factor-beta Type II; Receptors, Opioid, mu; Receptors, Transforming Growth Factor beta; Wound Healing; Wounds and Injuries

The chronic pelvic pain syndrome is a clinically defined symptom complex of unclear etiology. We have noted increased oxidative stress in the prostatic fluid of these patients, implying an active inflammatory response. Immune cells can produce the natural opioid beta-endorphin at the site of injury, which may modulate pain. We measured beta-endorphin and the inflammatory marker prostaglandin E2 in the expressed prostatic secretions of men with prostatitis, and correlated the results with symptoms.. Expressed prostatic secretions samples from 70 patients and 8 asymptomatic controls were collected and frozen. beta-Endorphin and prostaglandin E2 were measured by enzyme-linked immunosorbent assay. Results were stratified according to prostatitis category and compared in individuals before and after therapy.. In symptomatic patients beta-endorphin and prostaglandin E2 were not significantly different in categories II, IIIa and IIIb expressed prostatic secretions but they were higher than in controls. The mean beta-endorphin level plus or minus standard error of mean in symptomatic patients was significantly higher (23.8 +/- 11 ng./ml. versus 8.7 +/- 4.7, p = 0.0001) and mean prostaglandin E2 was lower (6.01 +/- 2.9 ng./ml. versus 3.01 +/- 2.9, p = 0.001) after successful therapy with antibiotics or antioxidant phytotherapy, Prosta-Q (Farr Laboratories, Santa Clarita, California).. We observed a correlation of higher prostaglandin E2 and lower beta-endorphin in symptomatic men with chronic prostatitis. Increased oxidative stress and inflammation may induce prostaglandin E2 production that would inhibit beta-endorphin release. Treatment with therapeutic agents that decrease oxidative stress, such as antibiotics and antioxidant phytotherapy, may function at least partially by increasing beta-endorphin and decreasing prostaglandin E2.

Topics: beta-Endorphin; Chronic Disease; Dinoprostone; Humans; Male; Oxidative Stress; Prostatitis

A limitation of current gene therapy efforts aimed at central nervous system disorders concerns distribution of vectors on direct injection into neural tissue. Here we have circumvented this problem by transferring genes to the meninges surrounding the spinal cord, achieving an in vivo gene transfer paradigm for treating chronic pain. The therapeutic vector consisted of a recombinant adenovirus encoding a secreted form of the potent endogenous opioid beta-endorphin. In an inflammation model of persistent pain, administration of the vector into the cerebrospinal fluid (CSF) surrounding the spinal cord transduced meningeal pia mater cells. The resulting increase in beta-endorphin secretion attenuated inflammatory hyperalgesia, yet had no effect on basal nociceptive responses. This demonstration of a gene transfer approach to pain treatment can be generalized to neurodegenerative disorders in which broad spatial distribution of therapeutic effect is critical.

Topics: Adenoviridae; Animals; beta-Endorphin; Chronic Disease; Genetic Therapy; Genetic Vectors; Injections, Spinal; Meninges; Pain Management; Paracrine Communication; Pia Mater; Rats; Transgenes

The aim of the present study was to investigate the effect of somatostatin administration in arthritic rats. Inflammation was induced by daily interplantar injection of 100 microl of Freund's complete adjuvant into the left hind paw of the rat. Arthritis developed 20 days following the first injection and was stable in the inoculate paw. Arthritic rats were treated interplantarly with somatostatin (5 or 10 microg) or with indomethacin (100 microg) daily for 14 days. Inflammatory response was studied at 12 h, 7 and 14 days following drug administration. The effect of somatostatin was determined by local (into popliteal lymph nodes) and systemic production of beta-endorphin. Our results showed that somatostatin treatment significantly increased beta-endorphin levels in the blood and lymphocytes from popliteal lymph nodes. Greater efficiency was seen when 5 microg instead of 10 microg of somatostatin was used. A significant decrease of absolute leukocytosis was observed at the 14th day following somatostatin administration. Moreover, a significant reduction of plasmatic beta-globulins at 12 h and the 7th day and of plasmatic alpha2-globulins at the 14th day was observed after the beginning of somatostatin treatment.

Topics: Alpha-Globulins; Animals; Anti-Inflammatory Agents, Non-Steroidal; Arthritis; beta-Endorphin; Beta-Globulins; Chronic Disease; gamma-Globulins; Indomethacin; Inflammation; Male; Pain; Rats; Rats, Wistar; Somatostatin

Topics: Animals; beta-Endorphin; Chronic Disease; Enkephalin, Methionine; Enkephalins; Gene Transfer Techniques; Genetic Therapy; Genetic Vectors; Humans; Mice; Pain Management; Protein Precursors; Simplexvirus; Spinal Cord

The chronic stage of vasospasm occurring several days after subarachnoid hemorrhage (SAH) is characterized by the development of histopathologic changes in cerebral arteries causing cerebral ischemia. Numerous experimental data indicate the involvement of immune mechanisms in the angiopathy caused by SAH. Endogenous opioids play also an important role in the ischemic lesions of the brain. Corticotropin releasing hormone (CRH) induces the release of beta-endorphin (beta-END) from hypothalamic neurons and also from mononuclear white blood cells. The function of CRH and beta-END in vasospasm following SAH and the interrelationship between neuroendocrine and immune changes requires further elucidation. In the present study we investigated the influence of CRH injected into cerebral cisterna magna (CM) of rats on beta-END-like level in cerebrospinal fluid (CSF) in acute and chronic phase of cerebral vasospasm following artificial SAH. Acutely CRH induced a significant rise of beta-END-like in CSF both in SAH and sham SAH rats. However, in rats subjected to SAH, a single injection of CRH caused a prolonged rise of 5-END in CSF, which was also seen 2 days after SAH, during the chronic phase of vasospasm. The obtained results indicate that CRH increases neuroendocrine changes induced by SAH, probably by an activation of immune cells involved in the patomechanism of chronic vasospasm.

Topics: Acute Disease; Animals; beta-Endorphin; Catheterization; Chronic Disease; Cisterna Magna; Corticotropin-Releasing Hormone; Male; Microinjections; Rats; Rats, Wistar; Subarachnoid Hemorrhage; Time Factors; Vasospasm, Intracranial

To assess the role of beta-EP in the physiological and pathophysiological process of respiratory regulation in chronic hypoxic rats.. The chronic hypoxic rat model was established by intravenous injections of papain 6 times, once a week. The concentration of beta-endorphin in medulla, pons, hypothalamus, central gray and plasma of chronic hypoxic rats were measured by radioimmunoassay. All animals were pretreated with sodium pentobartital (35 mg/kg) before experiment. 102 rats were randomly divided into three groups. Group 1 (n = 36). The respiratory rate (RR) and tidal volume (VT) were measured after intravenous injection of naloxone (NLX, 2 mg/kg), beta-EP (40 micrograms/kg, 160 micrograms/kg) or normal saline, Group 2 (n = 48). By the intracerebroventricular administration of NLX and beta-EP to the models, RR, VT and PaCO2 were observed after microinjection 5, 15, 30, 45, 60 min. Group 3 (n = 18). The respiratory effects of beta-EP after directly into the nucleus tractus solitari of the anaesthetised rats were investigated.. The beta-EP contents in medulla, pons, hypothalamus, central gray and plasma of chronic hypoxic rats were significantly increased compared with control subjects (P < 0.01). It suggested that the pathophysiology of chronic hypoxic process infleuced the contents of beta-EP in the CNS and plasma in rats. Intracerebroventricular microinjection of beta-EP in normal rats, resulted in a significant decrease in RR (P < 0.05). No significant difference in RR and VT was observved after intravenous injection of naloxone (2 mg/kg) and beta-EP (40 micrograms/kg, 160 micrograms/kg) in treatment group compared with the control group (P > 0.05), Intracerebroventricular microinjection of NLX in chronic hypoxic rats, resulted in a marked increase in RR (P < 0.05) and central hypercapnic-sensitivity (t = 2.76, P < 0.05), Intracerebroventriculalr microinjection of beta-EP in chronic hypoxic models, resulted in severe respiratory depression after injection 15, 30, 45, 60 min (RR t = 3.41, 6.54, 6.97, 7.87, P < 0.01; VT t = 3.07, 7.27, 6.14, 6.08).. These results indicate the beta-endorphin may be involved in central respiratory control of chronic hypoxic rats.

Topics: Animals; beta-Endorphin; Chronic Disease; Disease Models, Animal; Hypoxia; Male; Naloxone; Narcotic Antagonists; Oxygen; Rats; Rats, Sprague-Dawley; Respiration

This study was undertaken to investigate the effect of nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin.. Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG).. Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and nipradilol phases of the study. However, during the nipradilol phase, bradykinin did not change significantly at rest and at peak exercise.. Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.

Topics: Adrenergic alpha-Antagonists; Aged; beta-Endorphin; Bradykinin; Chronic Disease; Electrocardiography, Ambulatory; Exercise Test; Heart Rate; Humans; Male; Middle Aged; Myocardial Ischemia; Propanolamines; Radioimmunoassay

The aim of our study was to evaluate the effects of endogenous opioids on the secretion of atrial natriuretic factor (ANF) in moderate chronic heart failure (HF).. We evaluated the effects of i.v. volume load (NaCl 0.9% at 0.25 ml/Kg/min for 60 minutes) on heart rate (HR), on mean arterial pressure (MAP) and on the plasma levels of beta-endorphin (beta-end), met-enkephalin (Met-enk), dynorphin (Dyn), atrial natriuretic factor (ANF) and noradrenaline (NA) in 10 patients (age 58 +/- 9) with HF in NYHA class II (group I) and in 8 healthy control subjects (age 54 +/- 10) group II). The volume load was repeated after at least three days during infusion of naloxone (2 micrograms/Kg/min), evaluating the above mentioned hemodynamic and hormonal parameters.. The acute volume expansion caused an increase in ANF concentration (from 51.7 +/- 19.7 to 67.4 +/- 36.9 pg/ml; p < 0.05) and in beta-end (from 11.9 +/- 5.3 to 16.6 +/- 7.5 fmol/ml; p < 0.05), In group I. In group II an isolated increase in ANF was observed (from 14.1 +/- 7.8 to 21.9 +/- 7.9 pg/ml; p < 0.02). No significant changes were detected for HR, MAP, Dyn, Met-enk and NA. In group I the percent increase of ANF is less than in group II (30 vs 55%; p < 0.05). The volume load infused during naloxone infusion caused a significant increase in HR (from 73 +/- 6 to 78 +/- 9 bpm; p < 0.05) and in NA (from 311 +/- 123 to 415 +/- 142 pg/ml; p < 0.05) In group I. In group II, an increase in ANF was detected (from 13.8 +/- 6.0 to 23.6 +/- 5.0 pg/ml; p < 0.01).. Our data suggest that in moderate HF beta-end stimulates the secretion of ANF and inhibits the activity of the sympatho-adrenergic system during acute volume expansion.

Topics: Adult; Aged; Analysis of Variance; Atrial Natriuretic Factor; beta-Endorphin; Chronic Disease; Data Interpretation, Statistical; Dynorphins; Enkephalin, Methionine; Female; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Naloxone; Narcotic Antagonists; Norepinephrine; Plasma Volume; Receptors, Adrenergic; Sodium Chloride; Sympathetic Nervous System

Only little information is available on the effects of acute and chronic stress on the opioid and adrenergic systems in patients at intensive care units. Animal models showed a stimulation of beta-endorphin and catecholamines.. In the present study, in 12 patients who were intubated and were receiving artificial respiration because of cardiopulmonary resuscitation or primary respiratory failure, venous plasma concentrations of adrenaline, noradrenaline and beta-endorphin immuno-reactive material (IRM) were determined by a radioimmunoassay. In these patients, regular endobronchial suctioning was necessary. For inducing acute stress patients underwent three different methods of endobronchial suctioning or lavage.. In all patients concentrations of both adrenaline (529 +/- 117 pg/ml) and noradrenaline (2694 +/- 262 pg/ml) were increased above normal resting values. In 5 patients plasma beta-endorphin IRM concentration was below the detection limit, the other patients had beta-endorphin IRM concentrations above normal (26.65 +/- 3.80 pg/ml). Epinephrine (227 +/- 33 vs. 743 +/- 189 pg/ml; p < 0.01) and norepinephrine (1673 +/- 161 vs. 3423 +/- 368 pg/ml; p < 0.001) were significantly lower in the group with undetectable beta-endorphin IRM concentrations than in the group with detectable beta-endorphin IRM whereas heart rate was significantly higher (120/min vs. 99/min; p < 0.0003). beta-endorphin IRM concentrations were correlated negatively to heart rate (-0.55; p < 0.0005) and positively to the noradrenaline concentration (0.56; p < 0.0004). Artificially ventilated patients showed increased levels of beta-endorphin (19.27 +/- 3.16 pg/ml) as compared to the spontaneously breathing patients (13.29 +/- 4.34 pg/ml). Following acute stress due to endobronchial suctioning or lavage, blood pressure (150/70 mmHg vs. 172/81 mmHg; p < 0.01) and heart rate (107/min vs. 119/min; p < 0.005) increased in all patients, the other parameters did not.. It is concluded that beta-endorphin IRM concentration in the plasma is linked to epinephrine and norepinephrine concentrations under intensive care conditions. Endobronchial lavage or suctioning does not influence beta-endorphin IRM levels in plasma.

Topics: Acute Disease; Adolescent; Aged; beta-Endorphin; Blood Pressure; Bronchoalveolar Lavage; Cardiopulmonary Resuscitation; Chronic Disease; Consciousness; Critical Care; Epinephrine; Heart Rate; Humans; Middle Aged; Norepinephrine; Oxygen; Pulse; Respiration, Artificial; Respiratory Insufficiency; Sensitivity and Specificity; Stress, Physiological

Adjuvant-induced arthritis (AA) in specific strains of rats is an immunologically mediated inflammatory disease which is also characterised by activation of the endocrine system. To further investigate the effects of AA on processing of the pro-opiomelanocortin (POMC) precursor in rat immune tissues, we utilised radioimmunoassays for adrenocorticotrophin (ACTH), beta-endorphin and alpha-melanocyte-stimulating hormone (alpha-MSH) to measure these peptides in the spleen and thymus. 14 days following adjuvant injection, spleen levels of ACTH were elevated in the AA group (4.47 +/- 1.04 ng/g tissue, n = 9) compared to controls (2.42 +/- 0.4 ng/g) and exacerbation of the disease by removal of circulating glucocorticoids through bilateral adrenalectomy (ADX) resulted in further elevation of spleen ACTH (5.11 +/- 1.22 ng/g). beta-Endorphin levels in both the AA (10.60 +/- 1.61 ng/g) and AA/ADX (13.37 +/- 2.36 ng/g) groups were higher than controls (5.57 +/- 0.65 ng/g). Conversely, alpha-MSH spleen levels were decreased in the AA (2.89 +/- 0.22 ng/g) and AA/ADX (2.22 +/- 0.33 ng/g) groups compared to controls (4.62 +/- 0.45 ng/g) and were also decreased following adrenalectomy. In the thymus, ACTH levels were elevated in the AA group (8.95 +/- 1.41 ng/g) compared to controls (5.79 +/- 0.63 ng/g), and the same pattern was evident for thymic alpha-MSH (0.64 +/- 0.08 ng/g in AA animals compared to control levels of 0.35 +/- 0.03 ng/g). Following G50 gel filtration, ACTH and beta-endorphin immunoreactivities (ir) were present in both spleen and thymus as two peaks, one which eluted near the void volume and one which eluted in a lower molecular mass position than the standards.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenocorticotropic Hormone; alpha-MSH; Animals; Arthritis, Experimental; beta-Endorphin; Chronic Disease; Male; Pro-Opiomelanocortin; Rats; Rats, Sprague-Dawley; RNA, Messenger; Spleen; Thymus Gland

Chronic stress affects the reproductive function by modifying the neuroendocrine homeostasis. The aim of the present study was to clarify the neuroendocrine and the gonadal changes following chronic intermittent stress in male rats and the action of a neuroactive drug, acetyl-l-carnitine (ALC). The effect of two different stressors, cold water swimming or ether, on central beta-endorphin (beta-EP) and GnRH contents, and on plasma testosterone levels was investigated. In addition, the response to an acute stress in chronically stressed rats, treated or untreated with ALC (10 mg/day/rat p.o.), was evaluated. The stressors were applied twice a day for 10 days, and rats were killed before, during and after the last stress session. Mediobasal hypothalamus (MBH) beta-EP and GnRH contents, and plasma testosterone levels were evaluated by radioimmunoassay. The following results were obtained: (1) both chronic swimming and ether stress caused a decrease in hypothalamic beta-EP contents; (2) MBH GnRH contents increased after chronic swimming stress but not after ether stress; (3) chronic swimming stress induced a twofold decrease in plasma testosterone levels, while no changes were observed after ether stress; (4) the treatment with ALC prevented the decrease in plasma testosterone levels after chronic swimming stress, and (5) acute stress in chronically stressed animals caused an increase in MBH-beta-EP. The present data showed that chronic swimming stress reduces the reproductive capacity and impairs the capacity to respond to the acute stress and that ALC modulates the hormonal changes to physical stress and prevents the antireproductive effect of chronic cold swimming.

Topics: Acetylcarnitine; Animals; beta-Endorphin; Chronic Disease; Ether; Gonadotropin-Releasing Hormone; Hypothalamus; Male; Radioimmunoassay; Rats; Rats, Wistar; Stress, Physiological; Swimming; Testosterone

The authors systematically studied the release of the endogenous opioid peptides beta-endorphin and methionine (met)-enkephalin into the cerebrospinal fluid (CSF) during deep brain stimulation in patients suffering from otherwise intractable chronic pain. Nine patients were included in the study; six had stimulation electrodes placed in both the periventricular gray matter (PVG) and the thalamic nucleus ventralis posterolateralis (VLP) and three in the PVG only. Immunoreactivity of beta-endorphin and met-enkephalin (beta-EPir and MEir, respectively) was measured by radioimmunoassays in ventricular and lumbar CSF samples obtained before, during, and after stimulation. Prestimulation concentrations of beta-EPir and MEir were lower in ventricular than in lumbar CSF (6.6 +/- 0.5 vs. 13.7 +/- 1.0 pmol/liter, p = 0.0001, for beta-EPir; 33.6 +/- 5.1 vs. 48.3 +/- 3.2 pmol/liter, p < 0.05, for MEir). Ventricular CSF concentrations of both beta-EPir and MEir increased significantly during PVG stimulation, whereas VPL stimulation was without effect. No changes were seen in lumbar CSF levels of the peptides during stimulation in either site. A significant inverse relationship was found between the "during:before stimulation" ratios of visual analog scale ratings and beta-EPir levels during PVG stimulation. The beta-EPir and MEir concentration during:before stimulation ratios were positively correlated, whereas no correlation was present in prestimulation samples from ventricular or lumbar CSF. High-performance liquid chromatography of ventricular CSF pools obtained during PVG stimulation revealed that major portions of beta-EPir and MEir eluted as synthetic beta-endorphin and met-enkephalin, respectively, thus documenting the release of beta-endorphin and met-enkephalin into ventricular CSF during PVG stimulation. The finding of a direct relationship between beta-EPir release and pain alleviation may suggest a role for beta-endorphin in the analgesic mechanism of PVG stimulation.

Topics: Adult; Aged; beta-Endorphin; Chronic Disease; Electric Stimulation Therapy; Electrodes, Implanted; Enkephalin, Methionine; Evoked Potentials; Female; Humans; Male; Middle Aged; Pain Measurement; Pain, Intractable; Periaqueductal Gray; Thalamic Nuclei

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)

Topics: Acetylcarnitine; Animals; beta-Endorphin; Chronic Disease; Cold Temperature; Ether; Male; Pituitary Gland; Rats; Rats, Wistar; Stress, Psychological; Swimming

The immune system is important in the pathogenesis of vitiligo, and emotional stress has precipitated vitiligo in some patients. Opioid peptides, beta-endorphin, met-enkephalin, and alpha-melanocyte-stimulating hormone (MSH) act as immunomodulators, and their secretion increases during periods of stress.. To see whether these three neuropeptides might be related to vitiligo itself or to some alterations of the immune system in patients with vitiligo, we compared circadian variations in their plasma concentrations and natural killer cell activity of peripheral blood lymphocytes in 14 patients with vitiligo with those of 12 healthy subjects.. Plasma concentrations of neurohormones were evaluated by radioimmunoassay (immunoradiometric assay for beta-endorphin). Natural killer cell activity (NKCA) was assayed against K562 cells by 51Cr release technique. Data were compared by the Student t test and analyzed by cosinor analysis.. The NKCA in vitiligo patients was higher than in controls but had similar circadian rhythm. alpha-MSH had no circadian rhythm in controls or in patients; plasma alpha-MSH levels were the same. Daily met-enkephalin and beta-endorphin oscillations in patients were no longer circadian. beta-Endorphin plasma levels in stable vitiligo were higher than in controls. There were no differences between patients with active vitiligo and normal subjects. Met-enkephalin plasma levels were generally higher in vitiligo patients, especially in the one with active vitiligo, than in controls.. In vitiligo there are aberrations in neuropeptide, beta-endorphin, and met-enkephalin secretion. The plasma met-enkephalin level is positively correlated with the aggressiveness of the disease.

Topics: Adult; alpha-MSH; beta-Endorphin; Chronic Disease; Circadian Rhythm; Cytotoxicity Tests, Immunologic; Enkephalin, Methionine; Female; Humans; Killer Cells, Natural; Male; Middle Aged; Radioimmunoassay; Regression Analysis; Vitiligo

Previous studies have provided evidence of an increased sensitivity to pain, a decreased hypothalamic opioid tone, and decreased cerebrospinal fluid (CSF) beta-endorphin (beta-EP) concentration in patients with primary chronic headache. We applied separate specific radioimmunoassays for beta-EP in CSF and plasma on samples from age-matched controls and a group of 50 patients with chronic tension-type headache (CTH) fulfilling the diagnostic criteria set by the International Headache Society. Median CSF beta-EP concentrations (95% confidence limits) were 12.8 pmol/l (11.0-14.5) in CTH patients and 11.9 pmol/l (10.9-14.2) in the control group, which is not significantly different (P = 0.28). Plasma beta-EP concentrations did not differ either, being 3.1 pmol/l (2.4-3.7) and 3.3 pmol/l (1.8-4.0) in the patients with CTH and in controls, respectively (P = 0.88). Plasma and CSF beta-EP concentrations did not correlate. Reversed-phase high performance liquid chromatography (HPLC) of CSF pools from the headache patients and controls revealed similar profiles of beta-EP-immunoreactivity both when C-terminally and N-terminally directed antisera were used, suggesting a normal post-translational processing of the pro-opiomelanocortin gene in patients with CTH. beta-EP is not involved in the pathogenesis of CTH, or such a role is not reflected in CSF or plasma concentrations of the neuropeptide.

Topics: Adult; Aged; beta-Endorphin; Chromatography, High Pressure Liquid; Chronic Disease; Female; Headache; Humans; Male; Middle Aged; Pro-Opiomelanocortin

Alpha-N-acetyl-beta-endorphin (Ac-beta-EP) is a post-translational product of beta-endorphin (beta-EP) with no analgesic properties. Ac beta-EP is present in human fetal and adult pituitary gland and cross-reacts in all available beta-EP assays. This study evaluates levels of Ac-beta-EP in the cerebrospinal fluid (CSF) of 22 normal subjects and 15 chronic headache sufferers. Since dopamine may play a role in the acetylation process, homovanillic acid levels were also determined. After extraction and high performance liquid chromatographic (HPLC) fractionation of CSF, an immunoreactive Ac-beta-EP peak was detected coeluting with reference peptide. Ac-beta-EP was detectable in all but 5 normal subjects. In headache sufferers, Ac-beta-EP levels were always detectable and their mean value was significantly higher than that of healthy subjects (11.6 +/- 11.8 vs 3.9 +/- 3.6 fmol/ml; P less than 0.01). Conversely, CSF beta-endorphin (beta-EP) concentrations were decreased in headache patients (9.8 +/- 9.4 vs 15.7 +/- 9.7 fmol/ml; P less than 0.05), and as a consequence the beta-EP/Ac-beta-EP ratio was also markedly reduced (P less than 0.005). No difference was observed for CSF homovanillic acid concentrations. These data demonstrate that HPLC coupled to radioimmunoassay allows the identification of low but significant amounts of Ac beta-EP in human CSF. This compound represents a confounding factor when beta-EP immunoreactivity is assessed by conventional methods. In headache sufferers, Ac-beta-EP levels were higher than normal, whereas beta-EP concentrations were lower.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; beta-Endorphin; Chromatography, High Pressure Liquid; Chronic Disease; Female; Headache; Homovanillic Acid; Humans; Male; Middle Aged; Migraine Disorders; Muscle Contraction; Pain; Radioimmunoassay; Reference Values

Topics: Adenocarcinoma; Adrenocorticotropic Hormone; Anesthesia, Endotracheal; Anesthesia, Epidural; beta-Endorphin; Chronic Disease; Enkephalin, Leucine; Humans; Insulinoma; Intraoperative Care; Pain, Postoperative; Pancreatic Neoplasms; Pancreatitis; Postoperative Care; Stress, Physiological

Tumor Necrosis Factor-alpha/cachectin (TNF-alpha/cachectin), Lipopolysaccharide (LPS), ACTH, beta-Endorphin (beta-EPH), and Cortisol (F) levels were determined in 33 Headache patients: 22 patients were affected with Migraine (M) and 11 patients with Chronic Type Tension Headache (CTTH). TNF-alpha/cachectin serum level was detected in 15 out of 22 migraneous patients and in no CTTH patients. Plasma LPS was observed in 11 out of 15 TNF-alpha/cachectin positive migraneous patients (73%) and in 3 out of 11 CTTH patients (27%). A negative correlation was observed between TNF-alpha/cachectin values and either ACTH or beta-EPH. In the group of migraneous patients the presence of serum TNF-alpha/cachectin showed a sensibility of .6 and a specificity of 1. The endocrine and immunological implications concerning these data are discussed.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Chronic Disease; Endotoxins; Female; Headache; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Limulus Test; Male; Middle Aged; Migraine Disorders; Pituitary-Adrenal System; Tumor Necrosis Factor-alpha

Topics: Adrenocorticotropic Hormone; Back Pain; beta-Endorphin; Chronic Disease; Electric Stimulation Therapy; Electrodes, Implanted; Humans; Pain; Spinal Cord; Substance P; Time Factors

Beta-endorphin and beta-lipotropin plasma concentrations were evaluated in 24 patients with congestive heart failure (CHF) (10 patients had chronic CHF and 14 an acute episode superimposing on chronic CHF), and in 35 age matched controls. Beta-endorphin and beta-lipotropin were significantly lower (P less than 0.005 and P less than 0.001 respectively) in patients with CHF than in controls. A significant decrease of both peptides vs controls was observed also in the two subgroups of patients, with chronic and acute CHF, without statistical differences between the subgroups. Beta-endorphin and beta-lipotropin showed a close and significant correlation (r = 0.88, P less than 0.001) amongst the whole series of patients as well as in both subgroups with chronic and acute CHF. In consideration of the long duration of the disease the decreased concentrations of beta-endorphin and beta-lipotropin can be considered to be due to a depletion of the releasable pool of the peptides, as it was previously shown for chronic stress.

Topics: Acute Disease; beta-Endorphin; beta-Lipotropin; Chronic Disease; Female; Heart Failure; Humans; Male; Middle Aged

Concentrations of beta-endorphin in the cerebrospinal fluid were measured in 21 painless subjects and 37 patients with chronic pain. Statistical analysis of the results showed no significant difference between the two groups. This lack of correlation between beta-endorphin concentrations in the CSF and the presence of chronic pain highlights the difficulties and limitations encountered when trying to determine the role of endogenous opioid systems with this method.

Topics: beta-Endorphin; Chronic Disease; Humans; Pain, Intractable; Radioimmunoassay; Reproducibility of Results

The level of an endogenous opioid (peak B endorphin) was measured in chromatographically fractionated cerebrospinal fluid (CSF) sampled from two groups of chronic pain patients before and after intrathecal saline (placebo) injection. As assessed by a verbal rating scale, one group reported no change in their level of pain (non-responders, NR; n = 6) while the other group reported complete or greater than 50% pain relief (placebo responders, PR; n = 14). We find, as has been reported previously, that initial peak B levels were lower (by 50%) in these chronic pain patients' CSF than in CSF from pain-free (PF) normal controls (P less than 0.001, t-test). Peak B levels measured from CSF of the NR group undergoing this procedure did not change (P greater than 0.4, paired t-test). In contrast, a significant 2.3-fold increase was measured in the CSF peak B level of the PR group (P less than 0.05, paired t-test). This is the first direct evidence that a CSF opioid is correlated with placebo pain relief in chronic pain patients. Peak B is a potent analgesic substance when administered by the intracerebroventricular route in mice and its level is related to the patients' pain status in a presumably causal manner.

Topics: beta-Endorphin; Chronic Disease; Humans; Injections, Intraventricular; Pain; Placebos

The authors describe a new method of the treatment of patients with trigeminal neuralgias using electroconvulsive therapy. The method is based on the increase of beta-endorphin concentration as a result of electroconvulsive treatment. The treatment of 12 patients in accordance with the suggested method provided beneficial results and significant enhancement of the efficacy of therapy as compared to patients undergoing conventional treatment.

Topics: Adult; beta-Endorphin; Chronic Disease; Electroconvulsive Therapy; Female; Humans; Immunoglobulins; Leukocyte Count; Male; Middle Aged; T-Lymphocytes; Trigeminal Neuralgia

Twenty-five patients with chronic progressing multiple sclerosis were examined for the content of beta-endorphin in blood serum, supernatants of activated lymphocytes and CSF by RIA. At the same time the parameters of cellular immunity were appraised. Different relations were discovered between cellular immunity and the content of beta-endorphin in biological fluids which may play a material part in the pathogenesis of multiple sclerosis.

Topics: Adult; beta-Endorphin; Chronic Disease; Culture Media; Female; Humans; In Vitro Techniques; Interleukin-2; Leukocyte Count; Lymphocyte Activation; Male; Middle Aged; Multiple Sclerosis; Phytohemagglutinins; T-Lymphocytes

Beta-endorphin (B-Ep), ACTH plasma levels and cortisol serum levels have been evaluated by RIA, in 27 patients suffering from essential blood hypertension and in 20 healthy control subjects. The study was repeated in the hypertensive group after clonidine treatment for 15 days. B-Ep plasma levels were normal in the I stage of hypertension and did not show any significant difference in relation to the severity and duration of hypertension. ACTH and cortisol circulating levels in the hypertensive patients were in normal range. The increase of B-Ep plasma levels in the II and III stage of the hypertension is not modified by the reduction of blood pressure values; therefore it is unlikely linked to the elevated blood pressure, but probably to the vascular complications. Moreover, the results obtained after clonidine treatment seem to exclude that the hypotensive action of the drug is mediated by increment of B-Ep circulating levels.

Topics: Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; Blood Pressure; Chronic Disease; Clonidine; Drug Evaluation; Female; Humans; Hydrocortisone; Hypertension; Male; Middle Aged

Thanks to recent biochemical and neuroendocrine findings, migraine belonging to the group of primary headaches appears as a pathology of the antinociceptive system with evolutive character. It has been demonstrated, in fact, that right at the early stage of migraine, there is a significant reduction in liquoral concentrations of beta-endorphin (beta-E), endogenous opioid peptide followed by a similar change in the plasma opioid system. The opioid system deficiency is even more evident after stimulation tests that point to reduced reactivity of the hypothalamo-hypophyseal system with respect to stimuli that in normal subjects trigger hypophyseal beta-E incretion. Caffeine, a member of the methyl-xanthine group, is an interesting molecule in the study of migraine patients because the chronic intake of this substance, contained in numerous analgesics, has been related to the chronic nature of the pain. The purpose of the present study is to assess the relationship between caffeine consumption and plasma opioid system. With the administration of a single oral dose of caffeine, normal subjects present an increase in plasma concentrations of beta-E, while in patients with chronic migraine, the response is significantly lower. These data confirm the poor reactivity of the plasma opioid system to pharmacological stimuli in migraine. Average daily consumption of caffeine has also been determined. It was not possible to establish a correlation between consumption of caffeine and plasma concentrations of beta-E whether basal or after stimulus with caffeine.

Topics: Administration, Oral; Adult; beta-Endorphin; Caffeine; Chronic Disease; Female; Humans; Male; Middle Aged; Migraine Disorders

The content of gastrin, beta-endorphin, insulin, C-peptide in 129 patients with chronic gastric and duodenal diseases was studied by standard radioimmunoassay during the acute phase of the disease and after routine treatment. It is concluded that normalization of the hormonal homeostasis is one the criteria of treatment efficacy.

Topics: Adolescent; Adult; Aged; beta-Endorphin; C-Peptide; Chronic Disease; Duodenal Diseases; Female; Gastrins; Humans; Insulin; Male; Middle Aged; Peptides; Stomach Diseases

The effect of the combined preparation analgeton and its components--analgin (metamizol, noramidopyrindimethansulfonate) and aminton (2-amino-4-methyl-pyridinphosphate) was studied on the release of beta-endorphin and its influence on chronic hyperalgesia. Experiments were carried out in vivo and in vitro on white rats and it was established that analgin, aminton and analgeton stimulated the release of beta-endorphin, affecting various regulatory levels. Analgeton in contrast to analgin showed longer analgetic effect in animals with chronic hyperalgesia (adjuvant arthritis of white rats). Possibilities for pharmacological control of chronic pain by influencing the levels of endogenous opioids are discussed.

Topics: Aminopyrine; Animals; beta-Endorphin; Chronic Disease; Dipyrone; Drug Combinations; Hyperalgesia; Hyperesthesia; Male; Pain, Intractable; Picolines; Rats; Rats, Inbred Strains

A sensitive and specific radioimmunoassay for beta-endorphin without gel filtration of plasma extracts has been developed by using newly raised antibody. The minimal detectable quantity was 5 pg, and ED 50 was 23 pg/ml. The crossreactivity of antibody with beta-lipotropin was 3.3%, but not showed crossreaction with other fragments of beta-lipotropin, beta-MSH and ACTH. The inter-assay coefficient of variation was 2.7% to 17.4%, and the intra-assay coefficient of variation was 4.5% to 26.4%, respectively. The mean recovery for unlabeled beta-endorphin added to plasma and extracted was 92.1% to 110.4%. Plasma levels of beta-endorphin in 40 normal subjects was 14.7 +/- 3.1 pg/ml and 14.8 +/- 1.1 pg/ml in 10 patients with chronic glomerulonephritis whose renal function was normal. There was no significant difference between the two groups. On the other hand, plasma levels of beta-endorphin in 16 patients on maintenance hemodialysis was significantly increased of 56.3 +/- 6.3 pg/ml than the other two groups. Physiological role of this high beta-endorphinemia in patients on maintenance hemodialysis still remains to be resolved.

Topics: Adult; beta-Endorphin; Chronic Disease; Female; Glomerulonephritis; Humans; Male; Radioimmunoassay; Reference Values; Renal Dialysis

In this study the 24-h pattern of blood pressure (BP), heart rate (HR), plasma catecholamine (CA), beta-endorphin (beta-EP), beta-lipotropin (beta-LPH) and RIII threshold was investigated in a patient suffering from chronic paroxysmal hemicrania (CPH). The investigation was carried out before and during indomethacin therapy in order to assess the presence or otherwise of a disordered biorhythmic organization resembling that documented in cluster headache (CH). A severe alteration in the majority of the rhythms explored was found not only during the drug-free phase, but also in the indomethacin phase of the investigation. These data are similar to those obtained in CH studies and point to the possibility of a common pathophysiological mechanism.

Topics: Adult; beta-Endorphin; beta-Lipotropin; Blood Pressure; Catecholamines; Chronic Disease; Circadian Rhythm; Female; Hemodynamics; Humans; Indomethacin; Migraine Disorders

Abnormal content and proportion of leucin-and methionine-enkephalins and beta-endorphin were found in blood plasma of chronic colitis sufferers. Nonspecific ulcerative colitis was associated with relevant peptides deficiency varying with the disease gravity, whereas in catarrhal colitis the peptides concentration was significantly elevated. Endogenous opioid peptides seem to play a role in pathogenesis of various colitis forms.

Topics: Adult; beta-Endorphin; Chronic Disease; Colitis; Colitis, Ulcerative; Enkephalin, Leucine; Enkephalin, Methionine; Humans; Middle Aged

Cerebrospinal fluid (CSF) levels of B-endorphin (B-EP), B-lipotropin (B-LPH) and ACTH were measured in nine girls with Rett syndrome with features of autistic behavior (3.7-12.1 years of age) and in ten children with chronic leukemia (control group). The peptides were measured by radioimmunoassay, either directly in the sample (ACTH) or after Sephadex G-75 column chromatography, in order to eliminate interfering substances (B-LPH and B-EP). The CSF B-EP patient levels (20.8 +/- 13.1 fmol/ml, means +/- SD) were significantly lower than in age-matched controls (69.1 +/- 32.6, P less than 0.01), whereas the B-LPH and ACTH levels were in the control range. No correlations were found between the clinical findings and CSF neuropeptide concentrations. These data demonstrate a decrease in central opiate activity in girls with Rett syndrome.

Topics: Adrenocorticotropic Hormone; Autistic Disorder; beta-Endorphin; beta-Lipotropin; Child; Child, Preschool; Chronic Disease; Female; Humans; Leukemia; Syndrome

Thirteen patients with pain from various causes were treated by electroacupuncture for 30 min. Cerebrospinal fluid (CSF) was obtained before and after treatment. Opioid-like substances in the CSF were fractionated by high pressure liquid chromatography and assayed by competitive receptor binding using a mu-specific radioligand, [D-ala2, MePhe4, gly-ol5]-enkephalin (DAGO). Opioid activity, associated with a fraction, eluted at 18-20% acetonitrile, consistently showed an increase in level after acupuncture. Two other fractions eluted at larger concentrations of acetonitrile also increased significantly after acupuncture; however the increase was not consistently observed in every patient. Measurements of beta-endorphin and dynorphin by radioimmunoassay indicated that 80 and 60% of the patients, respectively, had a higher level of these peptides after acupuncture. The nature of the opioid activity, eluted at 18-20% acetonitrile is unknown; however a small amount of it could be found in various parts of the brain of rat.

Topics: beta-Endorphin; Chromatography, High Pressure Liquid; Chronic Disease; Dynorphins; Electroacupuncture; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Enkephalins; Humans; Pain; Pain Management; Radioimmunoassay

Topics: Acupuncture Therapy; Adolescent; Adrenocorticotropic Hormone; Adult; beta-Endorphin; Chronic Disease; Cyclic AMP; Dermatitis, Atopic; Female; Humans; Male; Middle Aged

Stress-inducing stimuli are associated with a suppression of immune function. In this study, the relationship between pituitary-adrenal hormone release and natural cytoxicity was examined in the rat during single and repeated instances of chronic stress. Increased plasma concentrations of both adrenocorticotropic hormone (ACTH) and beta-endorphin/lipotropin were correlated with increases in natural killer (NK) activity following a single period of immobilization. After 4 days of repeated daily immobilization (2.5 hours/day), the secretory response of beta-endorphin/lipotropin was similar to that on day 1, but NK activity was lower than on day 1. These observations suggest a complex interaction between pituitary-adrenal responses to stress and changes in natural cytoxicity.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; beta-Lipotropin; Chronic Disease; Corticosterone; Cytotoxicity, Immunologic; Killer Cells, Natural; Male; Rats; Rats, Inbred Strains; Reference Values; Restraint, Physical; Stress, Psychological

The purpose of this study was to assess the biochemical mechanisms underlying spinal cord stimulation (SCS). Seventeen patients with chronic pain were investigated by measuring cerebrospinal fluid concentrations of endogenous opioids and biogenic amines before and during dorsal column stimulation. Basal cerebrospinal fluid beta-endorphin levels were below the normal range. No significant change of norepinephrine, epinephrine, dopamine, beta-endorphin, beta-lipotropin, or adrenocorticotropic hormone levels were found after SCS. A 50% increase of cerebrospinal beta-endorphin and beta-lipotropin levels occurred in 6 out of 16 patients, namely those where SCS gave the major pain relief. These data confirm the derangement of the endogenous opioid system in chronic pain conditions and suggest that the beta-endorphin response to SCS could have clinical value in predicting the success of treatment.

Topics: Adult; Aged; Aged, 80 and over; beta-Endorphin; beta-Lipotropin; Chronic Disease; Electric Stimulation Therapy; Endorphins; Female; Humans; Male; Middle Aged; Neurotransmitter Agents; Pain; Pain Management; Spinal Cord; Statistics as Topic

Immunoreactive beta-endorphin (IR-BE) levels in the plasma, anterior pituitary (AP), the neurointermediate lobe of the pituitary (NIL), and the hypothalamus were determined in castrated female rats and castrated female rats treated with estradiol benzoate (estrogen), after exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute and chronic stress increased plasma levels of IR-BE to the same extent in castrated female rats and castrated female rats treated with estrogen. In castrated female rats, acute stress produced an increase in the concentration of IR-BE in the AP, which was attenuated by the administration of estrogen. Although IR-BE in the NIL was not influenced by acute stress in castrated animals, exposure to acute stress resulted in an elevation in IR-BE levels in the NIL of rats given estrogen. Chronic stress did not affect the concentration of IR-BE in the AP of castrated females or castrated females treated with estrogen. Chronic stress did, however, increase the concentration of IR-BE in the NIL of castrated animals. This affect of stress on IR-BE levels in the NIL was potentiated by estrogen administration. IR-BE levels in the hypothalamus were reduced by estrogen and were not affected by acute or chronic stress, regardless of the gonadal steroid environment. As determined by column chromatography, administration of estrogen, as well as subjection to chronic stress, promoted the processing of the proopiomelanocortin precursor to form beta-lipotropin rather than beta-endorphin in the AP. By these methods, the only immunoreactivity detected in the NIL and the hypothalamus was beta-endorphin. These data indicate that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization stress on IR-BE levels in the AP and the NIL and the effects of chronic immobilization stress on the levels of IR-BE in the NIL.

Topics: Acute Disease; Animals; beta-Endorphin; Chronic Disease; Estradiol; Female; Hypothalamus; Ovariectomy; Pituitary Gland; Rats; Rats, Inbred Strains; Restraint, Physical; Stress, Psychological

Beta-endorphin-like immunoreactivity was studied in 7 patients with algomenorrhea during pain attack and 15 minutes after alpha-tocopherol administration with a therapeutic aim (till the analgetic effect was reached). There was an increase in beta-endorphin-like immunoreactivity after alpha-tocopherol administration. Naloxone administration to 9 patients with algomenorrhea of various etiology resumed the pain. The effect of alpha-tocopherol application for pain relief depended on the pathogenesis of algomenorrhea. At the same time naloxone administration failed to resume the pain in patients, in whom alpha-tocopherol had a strong analgetic effect. It is assumed that the endogenous opioid system participates in alpha-tocopherol effect on pain relief in patients with algomenorrhea.

Topics: Adult; alpha-Tocopherol; Analgesia; beta-Endorphin; Chronic Disease; Dysmenorrhea; Endorphins; Female; Humans; Menstruation; Naloxone; Tocopherols; Vitamin E

Topics: Adolescent; Adult; Alopecia Areata; beta-Endorphin; Brain; Chronic Disease; Endorphins; Enkephalin, Leucine; Female; Humans; Male; Middle Aged; Neurotensin

The effects of short- and long-term neuroleptic therapy on peripheral secretion of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) were examined in 25 chronic schizophrenic patients. Haloperidol was given to 8 patients for 10 days (group A: 0.1 mg/kg b.w./day) and to another group of 8 patients for 30 days (group B: 10-18 mg/day). The other 9 patients were given a combination of haloperidol (6-30 mg/day) with either chlorpromazine (25-75 mg/day), clotiapine (40-60 mg/day), or fluphenazine decanoate (25-75 mg/month) for 14-18 months (group C). beta-EP and beta-LPH levels were assayed before and after each treatment. Haloperidol plasma levels were assayed in group B patients at the end of treatment. beta-EP mean basal levels were higher in patients than in controls; however, beta-LPH mean basal levels were higher only for group A patients. After treatment, the mean levels did not differ from those prior to therapy in groups A and B, while beta-LPH levels were significantly higher in group C. Level increases or decreases in single patients did not correlate with drug dose or duration of treatment, with baseline peptide levels or with the clinical effects of the various treatments.

Topics: Adult; Antipsychotic Agents; beta-Endorphin; beta-Lipotropin; Chlorpromazine; Chronic Disease; Dibenzothiazepines; Drug Therapy, Combination; Female; Fluphenazine; Haloperidol; Humans; Male; Middle Aged; Receptors, Opioid; Schizophrenia

Topics: Adult; beta-Endorphin; beta-Lipotropin; Bipolar Disorder; Chronic Disease; Circadian Rhythm; Depressive Disorder; Dexamethasone; Endorphins; Female; Humans; Insulin; Male; Middle Aged; Schizophrenia

To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive beta-endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF beta-endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.

Topics: Acute Disease; Aged; beta-Endorphin; Cerebral Infarction; Chronic Disease; Endorphins; Enkephalin, Leucine; Humans; Middle Aged; Radioimmunoassay

Plasma epinephrine (EPI), norepinephrine (NE), beta-endorphin, and corticotropin (ACTH) responses were measured during insulin-induced hypoglycemia in normal subjects and in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). In normal subjects, there was a striking rise in EPI, NE, beta-endorphin, and ACTH following the nadir of hypoglycemia. Both beta-endorphin and ACTH responses were significantly lower than normal in patients with MSA, in contrast to normal levels in IOH patients. No correlation was observed between the degree of adrenergic insufficiency and the beta-endorphin and ACTH responses. The normal peptide responses in IOH are consistent with involvement limited to the peripheral sympathetic nervous system, whereas lesions in the central nervous system in MSA interfere with release of beta-endorphin and ACTH in response to hypoglycemia. The strong correlation between beta-endorphin and ACTH levels is consistent with their common origin. Peripheral adrenergic activity is not essential for beta-endorphin and ACTH release in humans.

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Adult; Aged; Autonomic Nervous System Diseases; beta-Endorphin; Catecholamines; Chronic Disease; Endorphins; Female; Humans; Hypotension, Orthostatic; Hypothalamo-Hypophyseal System; Insulin; Male; Middle Aged; Shy-Drager Syndrome; Sympathetic Nervous System

The following data were obtained from 36 male chronic schizophrenics (ICD 295.6) of 47 +/- 11 years of age, treated with neuroleptics for the last 16 +/- 6 years: Age, age at first manifestation of disease, duration and dosage scheme of neuroleptic therapy and number of electroconvulsive shock treatments. Blood samples were drawn both under neuroleptic treatment and after a 12-day withdrawal of neuroleptics, for determining cortisol, prolactin, beta-endorphin and noradrenaline. Psychopathology was assessed by standard criteria via BPRS. In 27 patients CT determination was carried out to determine the breadth of the third ventricle and the ventricular brain ratio. Withdrawal of neuroleptics resulted in a marked improvement, whereas 11 patients showed pronounced deterioration of their psychotic symptoms. In respect of the entire group there was a significant improvement of anergy, while disturbances of thinking were significantly enhanced. Serum levels of beta-endorphin and cortisol increased after neuroleptic withdrawal, whereas the levels of prolactin and of noradrenaline dropped. A considerable proportion of the patients showed a distinct extension of the ventricular system, but the CT variables correlated only slight with psychopathological parameters or their changes after neuroleptic withdrawal. The other variables, too, were without clinically relevant prognostic importance compared with the psychopathological changes after neuroleptic withdrawal. These variables were e.g. demography, psychopathology, therapy and neuroendocrinology.

Topics: Adult; Antipsychotic Agents; beta-Endorphin; Cerebral Ventricles; Chronic Disease; Electroconvulsive Therapy; Endorphins; Hormones; Humans; Hydrocortisone; Male; Norepinephrine; Prolactin; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology; Substance Withdrawal Syndrome; Tomography, X-Ray Computed

Chronic arthritic pain was induced by intradermally inoculating rats at the tail-base with Mycobacterium butyricum, which results in swelling, inflammation, and hyperalgesia of the joints. These symptoms peak at 3 weeks after inoculation and disappear by 10 weeks. The following changes were seen at 3 weeks. Immunoreactive dynorphin (ir-Dyn) and ir-alpha-neo-endorphin (alpha-NE) manifested comparable patterns of change. Their levels were increased in the anterior, but not neurointermediate, pituitary. The thalamus showed a rise in ir-Dyn and ir-alpha-NE, but no alterations were seen in other brain regions. In each case, cervical, thoracic, and lumbosacral sections of the spinal cord showed a rise in ir-Dyn and ir-alpha-NE: This was most pronounced in the lumbosacral region, where the magnitude of these shifts correlated with the intensity of arthritic symptoms. In addition, a moderate elevation in ir-methionine-enkephalin (ME) was seen in lumbosacral spinal cord. In brain, ir was not changed. The level of ir-beta-endorphin (beta-EP) was elevated both in the plasma and the anterior, but not the neurointermediate, pituitary. In addition, the content of messenger RNA encoding the beta-EP precursor, proopiomelanocortin (POMC), was enhanced in the anterior lobe. Thus, there was a selective activation of synthesis of beta-EP in, and its secretion from, the anterior lobe. In no brain tissue did levels of ir-beta-EP change. At 10 weeks postinoculation, the above changes were no longer apparent, indicating their reversibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Arthritis; Arthritis, Experimental; beta-Endorphin; Brain; Brain Chemistry; Chronic Disease; Diprenorphine; Disease Models, Animal; Dynorphins; Endorphins; Hypothalamus; Male; Mesencephalon; Pain; Rats; Rats, Inbred Strains; Receptors, Opioid; Spinal Cord; Thalamus

Growing evidence indicates that most patients with coronary artery disease frequently have episodes of painless myocardial ischemia. Previous studies from our institution show that the severity and duration of myocardial ischemia are necessary but not sufficient factors to explain the occurrence of anginal pain. The responses to a battery of painful stimuli were studied in 12 patients with predominantly painless (group A) and in 15 patients with predominantly painful (group B) ischemic episodes. The severity of myocardial ischemia as assessed by the measurement of ST-segment depression during exercise stress testing and during ambulatory electrocardiographic monitoring was comparable in the 2 groups. Patients in group A had a significantly higher threshold and tolerance for forearm ischemia (+32%, p less than 0.05; +120%, p less than 0.001), cold (+100%, p less than 0.05; +180%, p less than 0.01) and electrical skin stimulation (+145%, p less than 0.01; +109%, p less than 0.01), but the overlap between the 2 groups was often appreciable. In the 6 patients with the longest tolerance times for forearm ischemic pain (all in group A) and in the 5 having the shortest tolerance times (all in group B), plasma levels of beta endorphin, met-enkephalin, noradrenaline and adrenaline were similar during both the basal state and the induction of forearm ischemic pain. Thus, a generalized defective perception of painful stimuli plays an important role in many patients with predominantly painless myocardial ischemia. Other mechanisms, however, may also be important, particularly in patients whose threshold and tolerance values overlap with those of patients who have predominantly painful myocardial ischemia.

Topics: Angina Pectoris; beta-Endorphin; Chronic Disease; Coronary Disease; Endorphins; Enkephalin, Methionine; Humans; Male; Middle Aged; Norepinephrine; Pain; Perception; Sensory Thresholds

The psychopathology of 36 chronic, schizophrenic patients who had been on maintenance neuroleptics was rated during neuroleptic therapy and after 12 days of neuroleptic withdrawal. At both times, hormonal serum levels were also determined. Moreover, in 27 of these patients, ventricle-brain ratio, maximal width of the third ventricle, and sulcal widening were measured on computed tomography (CT). Neuroleptic withdrawal resulted in individually different psychopathological changes: 7 patients improved, 11 worsened. Within the whole group, thought disorder deteriorated, and anergia improved. Levels of cortisol and beta-endorphin increased; those of prolactin and norepinephrine decreased. The majority of patients showed ventricular enlargement, which was marginally related to reduced thought disorder. CT and endocrine variables were slightly related to psychopathology or psychopathological effects of neuroleptic withdrawal.

Topics: Adult; Antipsychotic Agents; beta-Endorphin; Cerebral Ventricles; Chronic Disease; Endorphins; Humans; Hydrocortisone; Male; Middle Aged; Norepinephrine; Prolactin; Schizophrenia; Schizophrenic Psychology

The activation of the hypothalamic pituitary adrenal axis by stress is well-known. Using inescapable intermittent footshock as a stressor in rats, we have previously demonstrated a rise in circulating plasma Beta-endorphin/Beta-LPH which parallels the rise in plasma ACTH, the primary POMC derived peptides released by anterior lobe. In addition, the rise in ACTH is accompanied by approximately a tenfold rise in plasma corticosteroids. Short term anterior lobe pituitary cultures from rats who have received inescapable intermittent footshock for 30 minutes show a blunted dose response curves to the ACTH releasing secretagogues arginine vasopressin (AVP) and ovine corticotropin releasing factor (oCRF). Similarly a blunted dose response curves to secretagogues can be seen by either the addition of dexamethasone (0.5 nM) to the culture medium or pretreatment of the rats with 1 mg dexamethasone intraperitoneally 90 minutes prior to decapitation. Thus, glucocorticoids may play a role in the blunted response to secretagogues seen in anterior lobe cultures from acutely stressed rats. We now report that chronically stressed rats exhibit increased releasability of ACTH and Beta-endorphin/Beta-LPH products by oCRF, suggesting an increase of the peptides in the releasable pool.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; beta-Lipotropin; Chronic Disease; Corticotropin-Releasing Hormone; Dexamethasone; Endorphins; In Vitro Techniques; Male; Pituitary Gland, Anterior; Rats; Stress, Physiological

The role of opioid peptides in modulating the nervous system adaptability has been demonstrated recently; proopiomelanocortin (POMC)-related peptides, in particular, serve in pain perception, in adaptation to stress, and in modulating higher brain functions. Primary headaches, besides pain, involve neuroendocrine/autonomic/adaptive processes as well as mood and personality factors. The view that primary headaches can be taken as a possible model of POMC-related peptides dysfunction led us to evaluate the resting plasma and CSF peptide levels and their plasma changes in response to various stimuli affecting their release. The data obtained from basal and dynamic studies agree with the concept that primary headaches are sustained by opioid system disturbance. In particular the reduced release of endogenous opioids by anterior pituitary in response to physical, endocrine or pharmacological stimuli agrees with a weak adaptive ability of headache sufferers. This impairment of endorphin responsiveness could play a key role in headache susceptibility to environmental stimuli. Primary headaches constitute a wide, intriguing field, including several subgroups bordering on "ischemic" and behavioral/affective disorders. The development of neuroendocrine techniques could be a useful means for supporting the clinical criteria identifying subpopulations of headache sufferers.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Chronic Disease; Clonidine; Cluster Headache; Dexamethasone; Endorphins; Headache; Humans; Hydrocortisone; Middle Aged; Migraine Disorders; Pro-Opiomelanocortin

Topics: Adult; Animals; beta-Endorphin; Brain; Brain Chemistry; Cerebrospinal Fluid; Chronic Disease; Electric Stimulation Therapy; Endorphins; Humans; Middle Aged; Pain; Pituitary Gland; Rabbits; Spinal Diseases; Time Factors; Transcutaneous Electric Nerve Stimulation

Plasma concentrations of [met]enkephalin (ME) and beta-endorphin (beta E) were measured in samples obtained immediately before and after physiotherapeutic exercises for patients with ankylosing spondylitis (AS), osteoarthritis (OA), or knee injuries. Correlations were sought between opioid peptide concentrations or changes therein, and nature, severity and duration of disease, age, severity of pain reported and pain threshold. No correlation was found with any of the pain parameters. However, there was a possible relationship between age or duration of disease and changes in ME concentrations.

Topics: Adult; Aged; Arthritis; beta-Endorphin; Chronic Disease; Endorphins; Enkephalin, Methionine; Exercise Therapy; Female; Humans; Male; Middle Aged; Pain; Pain Management

Using radioimmunoassay the authors studied concentrations of beta-endorphine and metenkephalin in the cerebrospinal fluid (CSF) of 65 patients with various diseases of the central nervous system (CNS)--hereditary extrapyramidal disorders, disseminated sclerosis (DS), lateral amyotrophic sclerosis (LAS), spinal tumours, senile dementia, some CNS impairments of inflammatory nature. Patients with spinal tumours showed a 4-14-fold elevation in metenkephalin levels along with a comparatively high content of beta-endorphine. In senile dementia, the concentration of both peptides was lowered. In hereditary extrapyramidal diseases, the levels of beta-endorphine were also low, while there was no concomitant decrease in the metenkephalin concentration.

Topics: Amyotrophic Lateral Sclerosis; beta-Endorphin; Central Nervous System Diseases; Chronic Disease; Dementia; Endorphins; Enkephalin, Methionine; Humans; Multiple Sclerosis; Radioimmunoassay; Spinal Cord Neoplasms

Baseline plasma levels of beta-endorphin, beta-lipotropin, and ACTH were assayed in 37 patients with chronic schizophrenia: 24 men and 13 women, 28 with hebephrenic and nine with paranoid schizophrenia. None of the patients had received any medication for at least 10 days. The mean values of both opioids were significantly higher in the schizophrenic patients than in 21 age- and sex-matched control subjects. Insulin stimulation and dexamethasone suppression tests were given to eight of the patients, and the circadian rhythms of beta-endorphin, beta-lipotropin, ACTH, and cortisol were assayed in the same eight patients. Insulin stimulation, dexamethasone suppression test results, or circadian rhythmicity was impaired in seven of these eight patients.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Chronic Disease; Circadian Rhythm; Dexamethasone; Endorphins; Female; Humans; Insulin; Male; Middle Aged; Schizophrenia; Schizophrenia, Disorganized; Schizophrenia, Paranoid

Levels of beta-endorphin immunoreactivity in cerebrospinal fluid were measured in 12 chronic pain patients undergoing the surgical implantation of an electrode into the periventricular gray matter. Cerebrospinal fluid fractions were collected following placement of a cannula into the third ventricle, following injection of metrizamide contrast medium into the ventricles, following implantation of the electrode, and following electrical stimulation. A second set of samples was collected on a non-surgical day before and after stimulation. Levels of beta-endorphin immunoreactivity increased significantly from baseline levels to post-electrode implantation in one group of patients, but no significant change was seen following the onset of stimulation. Immunoreactivity increased significantly following metrizamide injection in a second group and was still elevated, in comparison to baseline, following electrode placement, but no increase was seen following the onset of stimulation. Levels of immunoreactive beta-endorphin did not increase in either group after stimulation on a post-surgical day, despite consistent reports of pain relief. Addition of metrizamide or a related contrast medium, iothalamate meglumine (Conray) to the beta-endorphin radioimmunoassay revealed that both compounds interfered with antigen-antibody binding and also quenched the gamma radiation emitted by iodinated peptide ligands. Due to these combined effects, the contrast media alone produced results similar to those of the beta-endorphin standard. Moreover, similar observations were made when contrast media were incorporated into radioimmunoassays for met-enkephalin, dynorphin and cholecystokinin octapeptide. These findings indicate that increased levels of beta-endorphin in cerebrospinal fluid are not directly associated with patient report of pain relief following periventricular gray stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: beta-Endorphin; Chronic Disease; Electronarcosis; Endorphins; Humans; Iothalamate Meglumine; Metrizamide; Pain Management; Radioimmunoassay; Thalamus

Topics: Adult; Aged; Analgesics; beta-Endorphin; Biological Availability; Chronic Disease; Endorphins; Female; Humans; Male; Middle Aged; Orosomucoid; Pain

Long-term stimulation of deep brain structures for pain relief has been efficacious in a significant number of patients who have been total failures at every other means of pain control. Two primary sites are used at this time--the periventricular grey area, which is related to the endogenous opiate system, and the internal capsule system, which is related to the dorsal column projection system. Periventricular sites are more efficacious for externally generated pain, that is, pain with input through the dorsal horn. Internal capsule stimulation is more efficacious for central nervous system-generated pain. While the preoperative preparation and intraoperative testing as well as postoperative testing of these patients requires a great deal of time and tedious attention to detail, our long-term results have been excellent using a combined comprehensive pain unit approach to pain and stress management, plus the stimulation techniques in carefully selected patients. Our results would indicate that initially 80-85% of patients get good pain relief, and then that range decreases to between 50 and 60% over a long period of time. Deep brain stimulation for pain relief is not a technique that should be used on a large number of patients with simple pain problems, but is highly efficacious in a selected group of patients with very specific pain problems that do not respond to usual pain treatment techniques. In patients with pain generated by benign etiologies, it is far superior to destructive procedures and does not have the secondary side effects of sensory loss, postchordotomy dysesthesias, or secondary neurological deficits.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: beta-Endorphin; Brain; Chronic Disease; Electronarcosis; Endorphins; Ganglia, Spinal; Humans; Pain; Pain Management; Prognosis; Serotonin; Spinal Cord; Stereotaxic Techniques

In twenty patients with chronic pain syndrome, acupuncture treatment resulted in significant improvement of both pain and psychiatric symptoms and higher plasma concentrations of metenkephalin. Plasma beta-endorphin concentrations were unchanged. The degree of symptom relief was correlated with the increase in plasma met-enkephalin.

Topics: Acupuncture Therapy; beta-Endorphin; Chronic Disease; Endorphins; Enkephalin, Methionine; Female; Humans; Male; Mental Disorders; Pain; Pain Management; Syndrome

This study compared basal concentrations of plasma beta-endorphin/beta-lipotropin-like immunoreactivity and dexamethasone suppression of cortisol in seven chronic pain patients, seven psychiatric disorder patients, and seven normal volunteers. Pain patients and psychiatric patients showed significantly higher basal concentrations of beta-endorphin/beta-lipotropin-like immunoreactivity compared to normal volunteers. Pain patients also had significantly higher beta-endorphin/beta-lipotropin-like immunoreactivity than psychiatric patients, even though there was no significant difference in severity of depressive symptomatology as assessed by Beck and Hamilton scores. Resistance to dexamethasone occurred in 57% of pain patients. These results may indicate that biological markers for depression occur in populations of chronic pain patients, or may reflect levels of central nervous system arousal in response to stress, pain, or nonaffective phenomena.

Topics: Adult; Alcoholism; beta-Endorphin; beta-Lipotropin; Chronic Disease; Depression; Dexamethasone; Endorphins; Female; Humans; Hydrocortisone; Male; Mental Disorders; Middle Aged; Mood Disorders; Pain; Radioimmunoassay; Syndrome

Topics: Aminooxyacetic Acid; Animals; beta-Endorphin; Brain Chemistry; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Chronic Disease; Endorphins; Ethanolamines; Liver Diseases; Male; Rats; Rats, Inbred Strains

Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.

Topics: Adult; beta-Endorphin; Brain Chemistry; Chronic Disease; Endorphins; Female; Headache; Humans; Male; Middle Aged; Migraine Disorders; Radioimmunoassay

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Chronic Disease; Endorphins; Female; Haloperidol; Humans; Male; Middle Aged; Mood Disorders; Schizophrenia

Eleven patients affected by common migraine (CM), eleven affected by daily chronic headache (DCH), and eight healthy volunteers were studied. Plasma levels of beta-endorphin (beta EP), beta-lipotropin (beta LPH). ACTH and cortisol were measured in basal conditions and after traditional Chinese acupuncture (TCA). Basal beta LPH and beta EP plasma levels (pg/ml) in the DCH patients (57.6 +/- 9.5 and 16.8 +/- 2.5, respectively; M +/- SE) were lower than those found in the controls (83.6 +/- 13.7 and 26.0 +/- 6.1; p less than 0.001), while those found in the CM cases showed inter-mediate values (75.3 +/- 12.0 and 24.4 +/- 5.8). ACTH and cortisol concentrations in both the CM and DCH patients were in the same range as those of the control group. TCA caused an increase in beta LPH and beta EP plasma concentrations in the control group (beta LPH: 117 +/- 16.9; beta EP: 44.1 +/- 6.7). Opioid plasma levels, however, remained unmodified after TCA in both the CM and DCH groups. ACTH plasma levels remained stable after TCA in all three subject groups. Patients suffering from primary headache are characterized by low beta LPH and beta EP plasma levels and by a poor reactivity of circulating opioids to non-stressful stimuli.

Topics: Acupuncture Therapy; Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Chronic Disease; Endorphins; Female; Headache; Humans; Hydrocortisone; Male; Middle Aged; Migraine Disorders