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 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

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

Silent--asymptomatic--ischaemia is one of the forms of ischaemic heart disease. Present possibilities of non-invasive diagnostics are based primarily on long-term ECG monitoring. With regards to the hypothesis that the raised algesic threshold at high level of analgetically reacting beta endorphins seems to be the pathophysiologic basis of this particular syndrome, we tried to verify the presumption by administering a beta-endorphin antagonist-naloxon. In 13 patients with a silent form of ischaemic heart disease (absence of stenocardia in objectively proved ischaemia in loading test) we made the loading test in a standard form and after administering of 2 mgs of naloxan intravenously. Owing to the fact that stenocardia developed only in one patient after endogenous opiate effect blockage we presume that pathophysiologic basis of this syndrome must be discovered elsewhere.
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PMID:[The role of beta-endorphins in silent forms of ischemic heart disease]. 252 92

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

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.
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PMID:Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris. 294 17

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms, 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exercise-induced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood samples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method). The mean baseline beta-endorphin plasma level was 22.5 +/- 19 pg/ml in patients with anginal symptoms compared with 43.7 +/- 28 pg/ml in asymptomatic patients (p less than 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups. Group II patients had a longer exercise duration (p less than 0.01), more pronounced ST segment depression (p less than 0.001) and a higher peak rate-pressure product (p less than 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups. These data suggest that higher baseline beta-endorphin plasma levels may play a role in the decreased sensitivity to pain in patients with silent myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.
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PMID:Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease. 296 73

Cardiac nociceptive afferences are mainly transmitted by sympathetic nervous tracts. After passing the ganglion stellatum and neighbouring ganglia, the nerves enter the dorsal horn of the spinal cord at C8-Th9 (especially Th2-Th6). Here the nerve synapses for the first time, mainly to neurons which run up to the thalamus contralaterally by the tractus spinothalamicus. Apart from atypically localised pain (jaw, head, neck), the nervus vagus is rarely involved in transmitting angina pectoris pain. There is no close relation between peripheral pain localisation and localisation of coronary stenosis or myocardial ischemia areas. The localisation of angina pectoris is decided by viscero-somatic summation (convergence-projection-theory). Almost all the ascending tracts of the tractus spinothalamicus with visceral inflow also receive inflow from somatic afferences, from skin areas of the dermatome from the same segment level, and especially from deep somatic structures such as muscle and ligaments (Head's zones). Additional reflex mechanisms, where the efferent part is probably sympathetic, explain transferred effects in the matching dermatome such as hypothermic skin zones, cutaneous hyperalgesia, higher pressure sensitivity of the muscles and occasionally even dystrophic changes. The amount of spinal visceral afferences is relatively small (only 1.5-2.5% of all somatic spinal afferences). The low amount, the pronounced divergence and, compared to converging somatic afferences, the larger receptive fields in the organ explain the diffuse, barely localisable character of angina pectoris pain. Cardiac afferences are tonically and phasically inhibited at spinal and supraspinal levels, especially by descending tracts. This explains why angina pectoris can be missing in spite of pronounced peripheral nociceptive impulse rates. Patients with silent myocardial ischemia have a higher central pain threshold than patients with symptomatic myocardial ischemia. Endogenous opioids are involved in the body's own analgesia system. The beta-endorphin level in the serum rises significantly in many patients during exercise diagnostic tests. Patients with silent myocardial ischemia have higher beta-endorphin levels compared to symptomatic patients at the same exercise level. This can be interpreted as expressing quantitative differences in a superior pain regulation system. Myocardial ischemia is experienced as angina pectoris pain when the peripheral nociceptive impulse rate is so pronounced that the prevailing inhibitory pain threshold can be overcome and when the pain pathways are intact.
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PMID:[Pain perception and peripheral pain localization in angina pectoris]. 306 37

Recently, more attention has been focused on the detection and treatment of silent myocardial ischaemia. Electrocardiographic signs of exercise-induced asymptomatic myocardial ischaemia are very common findings among survivors of acute myocardial infarction. From data of our population we found that silent exercise-induced ischaemia is present in 15-20% of all patients, and that about half of the patients with exercise-induced ST-segment depression were free of symptoms. Ergometric data at the ischaemic threshold are similar between asymptomatic and symptomatic patients while the presence of symptoms is more frequent in patients who were also symptomatic before the myocardial infarction. During the training period, the majority of the 'silent' patients remained asymptomatic, 23% developed effort angina, and 9% developed angina at rest. Training monitoring may be helpful in identifying the variability of symptoms. Physical training, in particular an intermittent programme, increased the work-load at which the ECG ischaemic signs appeared. Among the possible mechanisms responsible for exercise-induced silent ischaemia, a different pain tolerance and control of analgesia may be ascribed to explain the absence of pain, perhaps also determined by different endogenous beta-endorphin levels.
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PMID:Silent ischaemia in post-myocardial infarction patients submitted to physical training. 324 37

In a double-blind study, eight patients with symptomatic myocardial ischaemia and nine with asymptomatic myocardial ischaemia were compared during physical exercise under naloxone (6 mg i.v.) or placebo. Plasma beta-endorphin, cortisol and catecholamines were measured before exercise, during maximal exercise, and 10, 20 and 60 min after exercise. A tourniquet pain test (on the forearm, under control of transcutaneous PO2), and an electrical pain test (intracutaneous electrode placed in the finger with the electrical stimulus under computer control and two-interval forced-choice psychophysical technique) were performed before exercise as well as immediately after, and 60 min after exercise. Plasma beta-endorphin levels increased significantly (P less than 0.01) during exercise in symptomatic and asymptomatic patient groups; every patient showed an increase on beta-endorphins during and after exercise. However, the increase found in beta-endorphins during and after exercise was significantly larger (P less than 0.01) in asymptomatic than in symptomatic patients. After naloxone, this difference was no longer evident. Angina pectoris during exercise was reported with less latency in symptomatic patients (P less than 0.05) and occurred in two of nine asymptomatic patients following naloxone. The time course of plasma cortisol levels exhibited the same pattern as beta-endorphins with the same significant differences between symptomatic and asymptomatic groups. Electrical pain thresholds, though on average higher in asymptomatic patients (2.21 mA vs. 0.79 mA), were not affected by exercise or naloxone. Asymptomatic patients required more time to reach pain thresholds in the tourniquet pain test (P less than 0.02). After exercise, tourniquet pain thresholds were significantly lower (P less than 0.01) under naloxone compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of physical exercise on pain thresholds and plasma beta-endorphins in patients with silent and symptomatic myocardial ischaemia. 324 53


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