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

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

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

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

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

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

A study is presented of the blood plasma level of opioid peptides in patients with progressive stenocardia. Results indicate non-homogeneity of the patients concerning the content of neuropeptides. Two subgroups were singled out: 1. patients with progressive stenocardia of exertion in which beta-endorphin and leucin-enkephalin were above normal; 2. patients with a severe course of ischemic heart disease. Here the content of same peptides was lower than in the compared group. Similar dependence of changes of the content of methionine-enkephalin was not revealed.
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PMID:[Enkephalins and endorphins in unstable stenocardia]. 233 Jul 14


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