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)

A young Japanese female demonstrated unusual features of Cushing's syndrome, cardiac myxomas and mucocutaneous lentigines. At the age of 12 years she presented with growth failure and obesity. The dexamethasone suppression test, the metyrapone test and low corticotropin concentrations indicated a primary adrenal disorder. At surgery, the adrenal glands were not enlarged (the right, 4.0 g; the left; 4.5 g) but had numerous small dark brown nodules. The pathological findings showed multiple small black cortical nodules containing large cells with eosinophilic cytoplasm and lipofuscin, and internodular cortical atrophy. These abnormalities were consistent with primary pigmented nodular adrenocortical disease. At age 22 years she complained of fatigue and palpitations associated with mid-chest pain. Four cardiac myxomas, suspected from the echocardiogram, were surgically removed. Because Cushing's syndrome and cardiac myxomas are life-threatening conditions, an awareness of the complex is important.
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PMID:Cushing's syndrome due to primary pigmented nodular adrenocortical disease with cardiac myxomas and mucocutaneous lentigines. 160 Mar 14

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

The results of bicycle ergometry and pharmacological tests with isoproterenol and dipyridamol, 24-hour monitoring and blood levels of endogeneous opioids were studied in 99 females with chest pain who had undergone angiography. Coronary microcirculation was examined in 29 patients by introducing albumin microspheres into the left ventricle. The angiography revealed coronary atherosclerosis in 30 patients, whereas its signs were not found in 8 females with documented coronary heart disease (CHD). The predictive value of positive exercise tests in females with angina pectoris was higher for the diagnosis of CHD, including its types without coronary atherosclerosis. In patients with cardialgias, the predictive values of exercise tests were equally low for the diagnosis of coronary atherosclerosis, vasospastic and microvascular CHD types. The patients with cardialgias caused by autonomic dyshormonal myocardiodystrophy showed low blood beta-endorphin and leu-enkephalin levels.
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PMID:[Diagnostic usefulness of ECG changes in response to exercise in women with various forms of ischemic heart disease]. 175 7

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

Adrenocortical function, as reflected by sequential analysis of plasma cortisol and adrenocorticotropin (ACTH) test, was investigated in elderly patients (greater than or equal to 65 years) with acute myocardial infarction (AMI), and compared to young patients (less than or equal to 55 years) with AMI. Further, age-matched subjects admitted with ischaemic chest pain, in whom AMI was not verified, served as controls. Following infarction, plasma cortisol peaked within 24 hours in both age groups, whereupon the cortisol level gradually decreased till day 12. Plasma cortisol during AMI disclosed no age-related difference, but was significantly correlated to the localization of infarction and lactate dehydrogenase (LDH). The development of complications, i.e. hypotension, congestive heart failure, and arrhythmia, calling for therapeutic intervention, was solely correlated to infarct size, as estimated by peak LDH. Young and elderly patients responded equally and normally to ACTH stimulation, and in both groups a significant, positive correlation between the basal and the 30-min plasma cortisol was observed. Thus, we may conclude that in patients with AMI, the hypothalamic-pituitary-adrenocortical (HPA) response to stress and ACTH test shows no repression due to age.
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PMID:Adrenocortical function in old age as reflected by plasma cortisol and ACTH test during the course of acute myocardial infarction. 322 33

Whether i.v. infusion of beta-endorphin or metenkephalin can modify adenosine-provoked angina pectoris-like pain was investigated in healthy volunteers with a double-blind controlled design. All seven volunteers experienced dose-related adenosine-provoked chest pain. Metenkephalin did not modulate the dose-effect curve for adenosine while beta-endorphin counteracted (p < 0.01) the development of pain. The results suggest that peripheral p.subtype opioid receptors are involved in the modulation and may play a role in the genesis of silent and painful myocardial ischaemia.
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PMID:Beta-endorphin but not metenkephalin counteracts adenosine-provoked angina pectoris-like pain. 890 8

We have previously suggested that ozone (O3)-induced pain-related symptoms and inhibition of maximal inspiration are due to stimulation of airway C fibers (M. J. Hazucha, D. V. Bates, and P. A. Bromberg. J. Appl. Physiol. 67: 1535-1541, 1989). If this were so, pain suppression or inhibition by opioid-receptor agonists should partially or fully reverse O3-induced symptomatic and lung functional responses. The objectives of this study were to determine whether O3-induced pain limits maximal inspiration and whether endogenous opioids contribute to modulation of the effects of inhaled O3 on lung function. The participants in this double-blind crossover study were healthy volunteers (18-59 yr) known to be "weak" (WR; n = 20) and "strong" O3 responders (SR; n = 42). They underwent either two 2-h exposures to air or two 2-h exposures to 0. 42 parts/million O3 with moderate intermittent exercise. Immediately after post-O3 spirometry, the WR were randomly given either naloxone (0.15 mg/kg iv) or saline, whereas SR randomly received either sufentanil (0.2 microgram/kg iv) or saline. O3 exposure significantly (P < 0.001) impaired lung function. In SR, sufentanil rapidly, although not completely, reversed both the chest pain and spirometric effects (forced expiratory volume in 1 s; P < 0.0001) compared with saline. Immediate postexposure administration of saline or naloxone had no significant effect on WR. Plasma beta-endorphin levels were not related to an individual's O3 responsiveness. Cutaneous pain variables showed a nonsignificant weak association with O3 responsiveness. These observations demonstrate that nociceptive mechanisms play a key role in modulating O3-induced inhibition of inspiration but not in causing lack of spirometric response to O3 exposure in WR.
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PMID:Nociceptive mechanisms modulate ozone-induced human lung function decrements. 980 92

Adenosine is a neuromodulator with both excitatory and inhibitory effects dependent in part upon preconditions; it can act as an algesic or an analgesic agent. Previously we found variations of pain intensity during constant infusion of adenosine. We therefore quantified pain intensity during constant infusion of adenosine at a rate of 140 microg/kg/min intravenously in healthy volunteers, placebo controlled, double blind, and the relation to hemodynamic, vasomotor and sudomotor responses of the sympathetic nervous system and to the role of peripheral beta-endorphin response. The perceived chest pain during adenosine infusion showed an oscillatory pattern. Painful periods of about 30s were interrupted by painfree periods, and pain was always preceded by an increase in vasomotor sympathetic activity and by increased sudomotor activity. Plasma beta-endorphin values were heterogenous but exhibited an increase during infusion.
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PMID:Oscillation of pain intensity during adenosine infusion. Relationship to beta-endorphin and sympathetic tone. 1140 18