Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results from recent studies suggest that the endogenous opioid beta-endorphin (beta-E) is related to pain modulation. Therefore, plasma beta-E levels were studied in 23 patients with essential hypertension (EH) and in 7 patients with coronary artery disease (CAD) during asymptomatic ischemic events and in 5 patients with CAD during symptomatic ischemic events. Blood samples for beta-E were taken at the moment of silent ST depression, pointed with alarm by the real time ECG monitor "Q Med Monitor" (USA). Control blood samples were taken under the same conditions without ischemic events. Control plasma beta-E levels were significantly higher (p less than 0.01) in patients with EH as compared to that in both groups of patients with CAD (22.9 +/- 4.0 vs 7.0 +/- 1.9 and 4.5 +/- 1.6 pmol/l). At the time of silent ischemia, beta-E showed a significant increase in patients with EH (+10.1 +/- 2.1 pmol/l, p less than 0.01) and in patients with CAD (+10.7 +/- 1.3 pmol/l, p less than 0.05) as compared to the control levels. However, plasma beta-E showed no increase (+1.0 +/- 0.6 pmol/l, p greater than 0.1) during symptomatic ischemia as compared to the control levels. Thus, differences in the circulating levels of beta-E may be associated with the presence or absence of pain during myocardial ischemia.
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PMID:[Plasma beta-endorphin level in "silent" myocardial ischemia during Holter ECG monitoring]. 140 1

Plasma beta-endorphin levels provide controversial results on the role of endogenous opioid system in modulation of anginal pain. As an alternative, the action of plasmatic luteinizing hormone after administration of naloxone was investigated: naloxone blocks the tonic endogenous opioid system inhibition of gonadotropin release; thus, the level of luteinizing hormone after naloxone administration is an index of central endogenous opioid system activity. Twenty patients with coronary artery disease and positive results of stress tests were selected: 10 had angina (group I) and 10 did not (group II). Ten healthy subjects were also studied as a control group (group III). In all patients basal plasma beta-endorphin levels, basal luteinizing hormone plasma levels (every 15 minutes for 1 hour) and luteinizing hormone plasma levels after administration of 0.1 mg/kg naloxone over 4 minutes (every 15 minutes for 2 hours) were determined. In 15 patients the test was performed after luteinizing hormone releasing hormone was given. The integral concentration time of luteinizing hormone plasma level during baseline (LHiB) and after administration of naloxone (LHiN) or luteinizing hormone releasing hormone (LHiRH), the ratio (LHiN:LHiB and LHiRH:LHiB) and the differences (LHiN-LHiB and LHiRH-LHiB) between the postinfusion period and baseline were calculated. No difference was found in beta-endorphin plasma levels and luteinizing hormone response after luteinizing hormone releasing hormone infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous opioid system modulation in anginal pain: demonstration of its central activity. 151 84

To verify whether plasma beta-endorphin and bradykinin affects the pathophysiology of myocardial ischemia and the perception of cardiac pain, 35 patients with coronary artery disease were subjected to treadmill testing and 48-hour Holter ECG monitoring to measure their pain thresholds. Patients were divided into two groups during exercise testing: group 1 (N = 19) who had ST segment depression, and group 2 (N = 16), who had chest pain. Both groups were then compared with 12 age-matched control subjects. Pain thresholds were measured after Holter ECG monitoring, and blood samples were drawn before and immediately after exercise. No statistical differences were noted between groups 1 and 2 with regard to the severity of myocardial ischemia as assessed by ST segment depression or exercise tolerance time. The frequency of the episodes of silent myocardial ischemia in group 1 was found to be significantly (p less than 0.05) higher than that in group 2. The duration of the episodes of silent myocardial ischemia in group 1 was 41.9 minutes (range 3 to 343 minutes), which was significantly (p less than 0.05) longer than that in group 2 (11.5 minutes; range 0 to 74). The pain threshold in group 1 was a statistically (p less than 0.05) higher value than that in group 2. Although the resting plasma beta-endorphin level in group 1 was not statistically significantly different from values in either group 2 or the control group, during exercise the plasma beta-endorphin levels in both group 1 and the control group were significantly (p less than 0.05) elevated in comparison with their resting levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differences in plasma beta-endorphin and bradykinin levels between patients with painless or with painful myocardial ischemia. 173 63

To evaluate whether endogenous opioids (EO) play a role in the perception of anginal pain, a randomized double blind clinical trial, using naloxone (N) and placebo (P) and measuring beta-endorphin (beta-ep) plasma levels, was performed. We studied 10 patients with angiographically assessed coronary artery disease (CAD) and stable exercise-induced myocardial ischemia (established by 2 preliminary bicycle ergometric tests) of whom 5 symptomatic (SYM) and 5 asymptomatic (ASYM) and 5 subjects without CAD as a control group (CON). On a third exercise test the beta-ep plasma level (fmol/ml) was measured at rest (SYM 5.4 +/- 2.3 vs ASYM 7.2 +/- 2.3 vs CON 6.8 +/- 2.6, NS), at peak exercise (SYM 4.4 +/- 1.8 vs ASYM 8.0 +/- 4.2 and vs CON 6.2 +/- 2.7, NS) and during recovery (SYM 7.5 +/- 4.2 vs ASYM 7.2 +/- 3.0 vs CON 6.7 +/- 2.5, NS). On 2 subsequent tests patients received N (0.2 mg/kg) or P intravenously and chest pain was evaluated on an analogue scale (score from 1 to 10). After N compared to P we observed: an increased perception of chest pain in SYM (6.8 +/- 1.5 vs 4.2 +/- 1.0; p less than 0.01) without significant changes of the ischemic threshold (total work, heart rate-blood pressure product, ST segment changes, 2D-echocardiographic wall motion abnormalities); no modifications in ASYM and CON.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of endogenous opioids on nociceptive threshold in patients with exercise-induced myocardial ischemia. 191 14

The hypothesis that endogenous opioids may be involved in reduced exercise-induced ischemic pain or in silent ischemia was tested. Fifteen male patients with coronary artery disease were tested in a randomized, double-blind crossover study. After a preliminary screening effort test they were divided into two groups: the first group of nine patients received an i.m. injection of naloxone 0.4 mg, or saline as placebo, and the second group, comprising six patients, received 4 mg naloxone or saline i.v. Effort testing was performed at weekly intervals on an ergometric bicycle, following the Bruce protocol. ECG, heart rate, blood pressure and pain perception were monitored continually. Blood was sampled through an indwelling venous catheter for beta-endorphin determination before, at the peak of, and 10-20 min following exercise. ST depression, heart rate, blood pressure and the double product were similar after naloxone and following saline administration. Beta-endorphin concentrations in plasma were significantly increased following exercise in the second group of patients. The increase in beta-endorphin concentration was larger when the patients were pretreated with naloxone (4 mg) than with placebo. However, chest pain was not significantly altered by either dose of naloxone.
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PMID:Asymptomatic or mildly symptomatic effort-induced myocardial ischemia: plasma beta-endorphin and effect of naloxone. 213 95

Today silent myocardial ischemia (SMI) is a well-recognized phenomenon. However, in the absence of clinical signs suggesting coronary artery disease (CAD), a streamlined diagnostic approach for precise clarification has proved to be difficult. Sensitivity and specificity of ergometric results are rather poor in symptom-free patients. Thus the question arises, whether the necessity of coronary angiography can be established more precisely by 201Tl myocardial SPECT in these patients. Treadmill exercise according to the Bruce protocol, 201Tl myocardial SPECT and coronary angiography were performed in a total of 106 patients with suspected SMI. In group I (high probability of ischemia; n = 46), reversible defects detected by SPECT correlated well with significant stenoses and irreversible defects with subtotal stenoses or complete occlusions. SPECT sensitivity in the detection of ischemia was 91%, its specificity 96%. In group II (low probability of ischemia; n = 60), SPECT sensitivity was as high as in group I (94%) but due to a high number of false-positive results (e.g. cardiomyopathy) specificity was only 75%. However, SPECT was superior to exercise ECG (sensitivity 70%; specificity 56%) in the detection of SMI. In addition, beta-endorphin levels were determined in 180 healthy subjects, 37 patients with symptomatic CAD and in 34 patients with SMI before and during maximum exercise. Exercise values in patients with SMI were significantly higher than in healthy subjects or in patients with symptomatic CAD.
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PMID:201Tl myocardial SPECT and beta-endorphin levels in patients with suspected silent ischemia. 221 10

Two invasive studies (invasive study I and invasive study II) showed positive effects of transcutaneous electrical nerve stimulation (TENS) in pacing-induced angina pectoris in terms of increased tolerance to pacing, improved lactate metabolism and less anginal pain. Invasive study I demonstrated a decrease in left ventricular afterload by TENS treatment as reflected by a fall in systolic blood pressure, and this fact was thought to be explained by reduced sympathetic activity since arterial levels of epinephrine and norepinephrine dropped during TENS in TENS responders. In invasive study II, the influence of naloxone on the effects of TENS in pacing-induced angina pectoris was studied in 11 patients with severe coronary artery disease. The patients were catheterized and treated with TENS on 2 occasions; one with a single intravenous (i.v.) dose of saline as placebo and one with a single i.v. dose of 50 mg naloxone, double-blind, in random order. Treatment with TENS increased tolerance to pacing (P less than 0.01 with placebo and P less than 0.01 with naloxone, respectively) and improved lactate metabolism (P less than 0.05 with placebo and P less than 0.01 with naloxone, respectively). The positive effects of TENS were thus reproducible and not reversed by single i.v. doses of naloxone. The results of this study indicate that the effects of TENS on the heart are not mediated by beta-endorphin but do not exclude activation of more short-acting opioids like delta or kappa receptor agonists (met-enkephalin and/or dynorphin) since naloxone has a low affinity for these receptors. It is also possible that non-opioid mechanisms are of importance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of transcutaneous electrical nerve stimulation (TENS) on catecholamine metabolism during pacing-induced angina pectoris and the influence of naloxone. 235 62

As is obvious from the previous discussions, obesity is associated with a wide variety of changes in endocrine parameters (Table 1). Some of these changes, such as the reduction in SHBG without change in serum free testosterone levels, reflect merely laboratory abnormalities that may influence interpretation of diagnostic tests but have no important physiologic relevance. Other abnormalities have major clinical impact, such as hyperestrogenemia-endometrial carcinoma and hyperlipidemia-coronary artery disease. In some cases, endocrine changes in obesity are beneficial--that is, hyperestrogenemia leading to lower incidence of osteoporosis. In other cases, such as the profound suppression of growth hormone output in obesity, the physiologic relevance is unknown. Several endocrine changes in obesity, such as the impaired response of many hormones (growth hormone, prolactin, vasopressin, corticotropin) to insulin-induced hypoglycemia and elevated endorphin levels, suggest hypothalamic dysfunction. Furthermore, the failure of all of these abnormalities to be normalized after weight reduction raises the possibility of an underlying disorder leading to both endocrine dysfunction and obesity, rather than the endocrine dysfunction being simply a consequence of the obesity. Successful elucidation of the pathogenesis of obesity, which might then lead to much needed specific treatment modalities, may be advanced if we can solve some of these puzzles.
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PMID:Endocrine aspects of obesity. 264 1

The influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing was studied in 11 patients with severe coronary artery disease. The patients were catheterised and treated with transcutaneous electrical nerve stimulation on two occasions, double blind and in random order, with a single intravenous dose of saline or with a single intravenous dose of 50 mg naloxone. Treatment with transcutaneous electrical nerve stimulation increased tolerance to pacing and significantly improved lactate metabolism with placebo and with naloxone. The positive effects of transcutaneous electrical nerve stimulation were thus reproducible and not reversed by single intravenous doses of naloxone. The results indicate that the effects of transcutaneous electrical nerve stimulation on the heart are not mediated by beta endorphin but they do not exclude activation of more short-acting opioids such as delta or kappa receptor agonists (met-enkephalin or dynorphin or both) because naloxone has a low affinity for these receptors. Non-opioid mechanisms may also be important.
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PMID:Influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing. 278 1

The reason for the absence of pain perception in silent myocardial ischemia is unknown. A role of increased endorphinic activity in patients with silent ischemia has been postulated. To further investigate this hypothesis, 10 men with documented coronary artery disease and previous positive electrocardiographic findings during exercise without anginal pain were studied. Six healthy volunteers served as control subjects. The protocol included 2 bicycle exercise tests, the first test serving as baseline and the second performed after administration of naloxone, a specific opiate antagonist. Plasma beta-endorphin levels were measured by radioimmunoassay in both tests at rest, at peak exercise level and after recovery. All patients underwent thallium-201 scintigraphy after coronary vasodilation to provide an additional independent marker of ischemia. All patients showed stress-induced reversible perfusion abnormalities. No patient reported pain after naloxone application. Exercise duration, blood pressure and heart rate were not significantly altered by naloxone. Plasma beta-endorphin levels ranged from 18 +/- 6 pg/100 microliters (mean +/- standard deviation) at rest to 22 +/- 6 pg/100 microliters during exercise in the patient group and from 20 +/- 5 to 27 +/- 9 pg/100 microliters in the control subjects. Thus, there was no significant increase of plasma beta-endorphins during exercise or after naloxone administration, nor was there any difference observed between patients and control group. These data support the view that endorphinic activity does not play an essential role in the pathophysiology of silent myocardial ischemia.
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PMID:Role of beta-endorphins in silent myocardial ischemia. 294 65


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