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)

In this study we assessed the role of psychological factor in the etiology of coronary vasospasm using the Cornell Medical Index (CMI), focusing attention on the relationship between stress and serum magnesium (Mg). The study subjects consisted of 25 patients with variant angina (VA), 32 with old myocardial infarction without vasospasm (OMI), and 34 healthy men (controls). On a neurosis-discriminative diagram of CMI, areas I and II were considered as normal and areas III and IV were considered to be a neurotic disorder. The stress test included exercise and a quiz. Exercise test was performed in 8 patients with VA, 6 with OMI, and 5 controls, and a quiz was given to 4 patients with VA. Plasma catecholamines [noradrenaline (NA), adrenaline (Ad), dopamine], aldosterone, adrenocorticotropic hormone (ACTH) and serum electrolytes (Mg, Ca, Na, K, Cl) were measured before and after exposures to stress. The following results were obtained: 1) Of the patients with VA, 40.0% were categorized as area III or IV, compared to 18.7% of the patients with OMI, and 2.9% of the control subjects. 2) Among patients with VA, 64.0% exhibited anxiety states compatible with a psychological disorder. 3) NA and Ad were increased after exercise stress. 4) Serum Mg and Ca were also increased after exposure to exercise stress in all groups, and the degrees of these changes were correlated to the exercise intensity. The %delta Mg/%delta NA ratio, a parameter of the effect of catecholamine on the serum Mg, was greater in patients with VA than in those with OMI and the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The relation of physical and mental stress to magnesium deficiency in patients with variant angina]. 133 93

Thirteen patients with totally silent myocardial ischemia (group 1) and 15 patients with effort angina (group 2) were studied. The coronary angiography of both groups indicated coronary artery stenosis > or = 50%. In group 1, the beta-endorphin plasma level (beta-EPL) during rest was significantly higher than those in group 2 (15.639 +/- 1.258 pg/ml and 8.920 +/- 1.478 pg/ml, respectively, P < 0.01). There were significant increases in beta-EPL in both groups after exercise as compared with that before exercise (beta-EPL is 33.801 +/- 6.243 pg ml/in group 1, P < 0.01; 18.169 +/- 3.540 pg/ml in group 2, P < 0.01). The difference between two groups after exercise was also significant (P < 0.05). The plasma level of noradrenaline (NE) during rest was 0.267 +/- 0.035 ng/ml, adrenaline (E) was 0.112 +/- 0.018 ng/ml in group 1, and NE was 0.218 +/- 0.032 ng/ml and E was 0.110 +/- 0.015 ng/ml in group 2. After exercise, NE was 1.017 +/- 0.160 ng/ml (P < 0.001), E 0.276 +/- 0.076 ng/ml (P < 0.001), E 0.260 +/- 0.043 ng/ml (P < 0.01) in group 2. There was no difference between two groups both in rest and after exercise (P > 0.05). This study indicates that the high plasma beta-endorphin level might play a major role in the occurrence of totally silent myocardial ischemia.
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PMID:[Assessment of plasma catecholamine and beta-endorphin contents in patients with silent myocardial ischemia and angina pectoris]. 147 88

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

We measured substance P-like immunoreactivity (SPLI), beta-endorphin-like immunoreactivity (BELI), acetylcholinesterase activity, and total protein content in pericardial fluid and plasma of patients with angina pectoris and patients with no angina pectoris. SPLI and BELI levels, acetylcholinesterase activity, and total protein content were determined by radioimmunoassay, a colorimetric method, and by the method of Lowry et al. (J Biol Chem 1951; 193:265-75), respectively. In the pericardial fluid, patients with angina had SPLI, BELI, acetylcholinesterase, and total protein values of 1.69 +/- 0.23 fmol/mg protein, 0.16 +/- 0.13 fmol/mg protein, 0.06 +/- 0.02 units, and 25.7 +/- 3.2 mg/ml, respectively. Patients with no angina had SPLI, BELI, acetylcholinesterase, and total protein values of 0.93 +/- 0.17 fmol/mg protein, 0.19 +/- 0.10 fmol/mg protein, 0.16 +/- 0.02 units, and 44.6 +/- 5.3 mg/ml, respectively. SPLI levels were significantly higher (p less than 0.03), and acetylcholinesterase (less than 0.002) and total protein content (less than 0.004) were significantly lower in the pericardial fluid of patients with angina when compared with those of patients with no angina. BELI levels were not significantly different between the two groups. In the plasma, no significant differences were found in SPLI, BELI, acetylcholinesterase, and total protein values between the two groups of patients. Patients with angina had SPLI, BELI, acetylcholinesterase, and total protein values of 0.47 +/- 0.26 fmol/mg protein, 0.06 +/- 0.06 fmol/mg protein, 0.29 +/- 0.15 units, and 68.2 +/- 8.7 mg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substance P, acetylcholinesterase, and beta-endorphin levels in the plasma and pericardial fluid of patients with and without angina pectoris. 170 48

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

A sample of 45 patients with a history of coronary heart disease and documented myocardial ischemia during exercise testing were evaluated in an investigation of the possible relationships between psychological factors (depression and Type A behavior pattern), plasma beta-endorphin response and pain experience during maximal exercise-induced ischemia. Depression was assessed using the MMPI-D subscale, while Type A was evaluated using the Structured Interview. All patients developed ischemia during exercise as defined by ST-segment depression; however, only 18 patients reported anginal pain. Patients with high depression scores (MMPI-D greater than or equal to 70; n = 13) showed lesser increases in plasma beta-endorphin levels, tended more often to report anginal pain and rated pain as more severe during exercise than patients with low depression scores (MMPI-D less than 60; n = 18). Hemodynamic responses and severity of ischemia (assessed by ejection fraction changes and wall-motion abnormalities) did not differ between depression groups. Even after adjustment for group differences in exercise duration, depression was significantly associated with a lesser beta-endorphin response in the sample as a whole and, among patients reporting angina, with earlier pain onset and greater pain duration and severity. In contrast, when Type A versus B/X subgroups were compared, no differences in pain experience, beta-endorphin response or measures of ischemia were obtained. These findings suggest that in patients with ischemic heart disease, there may be a relationship between depression and anginal pain which may in part involve a blunted or absent beta-endorphin response.
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PMID:Depression and type A behavior pattern in patients with coronary artery disease: relationships to painful versus silent myocardial ischemia and beta-endorphin responses during exercise. 175 50

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 situation of absent pain with silent myocardial ischemia is highly difficult to define. There are probably several reasons for the lack of pain. Partly, nerve ways may be destroyed, partly, myocardial ischemia as peripheral pain stimulus may be to weak and beyond threshold, however, additionally, there are a lot of clues for the participation of endogenous pain modification systems therein. A certain amount of myocardial ischemia is a necessary, but not sufficient precondition for anginal pain. Myocardial ischemia is only felt painfully if the peripheral nociceptive impulse rate is high enough to pass the actual inhibitory pain threshold, and if the nerve ways are intact. It is generally accepted that the endogenous opiate system, to some extent, takes part in the endogenous analgesia system. A range of examinations in recent years hinted at the fact that endorphins are in relation to the absence of pain in silent ischemia. Patients with symptomatic and asymptomatic myocardial ischemia are significantly different in plasma beta-endorphin levels at rest and during physical exercise. A relation between peripheral endogenous opiates and suffering behavior can, at present, only be indicated correlatively. It is likely that the intensive overlaying of the cardiovascular and pain regulating systems is related to the absence of pain in silent myocardial ischemia.
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PMID:Influence of opiate systems in pain transmission during angina pectoris. 196 35

Plasma beta-endorphin (beta-END) levels were measured before, after exercise tests and at the onset of spontaneous angina in 23 anginal patients (group 1), 23 patients with silent myocardial ischemia (group 2) and 15 healthy volunteers (group 3). The pain perception in three groups was also measured. Before and after exercise, the concentration of beta-END in group 1 was significantly lower than that in group 2 and group 3. The concentration of beta-END during onset of spontaneous angina was also lower than that of angina-free period in group 1. There was no significant difference of beta-END between group 2 and 3. The values of the pain threshold and tolerance in group 1 were lower than those of group 2 and 3. These data suggested that plasma levels of beta-END may be related to occurrence of angina. The anginal patients had a hypersensitivity and hypotolerance for pain. A positive correlation was found between plasma beta-END and pain threshold, the levels of beta-END might affect the pain perception during the onset of myocardial ischemia.
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PMID:[The role of beta-endorphin and pain perception in silent myocardial ischemia]. 206 Apr 63

The role of increased beta-endorphin activity in patients with silent myocardial ischemia has been postulated. To further investigate this hypothesis, 13 patients with silent myocardial ischemia (A) and 10 patients with exercise-induced angina (B) were studied. To be entered in groups A and B patients had to fulfill the following criteria: occurrence or not of anginal pain, according to history and clinical data, during a positive exercise ECG and associated imaging of reversible perfusion defect at thallium-201 scintigraphy. Basal plasma beta-endorphin levels showed significantly (p less than 0.05) higher values in group A as compared to group B. At the end of an exercise stress test, plasma beta-endorphin levels were measured in 9 patients from group A and in 7 from group B. Post-exercise beta-endorphin levels showed a mild increase in group A, but increased significantly in group B (p less than 0.02). The patients with silent or symptomatic myocardial ischemia were quite well-matched with regard to age, sex, number and localization of obstructed coronary vessels, positive exercise ECG and imaging of reversible perfusion defect at thallium-201 scintigraphy. The higher basal plasma beta-endorphin levels in patients with painless ischemia, compared to symptomatic patients, suggested that endogenous opioid peptides play a role in the perception of anginal pain during myocardial ischemia. The fact that post-exercise plasma beta-endorphin levels increased in symptomatic patients but remained unchanged in patients with silent myocardial ischemia does not lead to conclusive considerations.
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PMID:[Plasma beta-endorphin levels in silent or symptomatic myocardial ischemia]. 224 56


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