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)

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

Myocardial ischemia can manifest itself as strictly silent or a combination of symptomatic and silent episodes. We have demonstrated that most asymptomatic patients have a higher threshold for pain than did symptomatic patients. Low sensitivity to pain in patients with silent ischemia may be related to both a neural pain inhibitory system and the release of endogenous opiates, the endorphins. beta-Endorphin release occurs during and after exercise; patients with asymptomatic ischemia had higher plasma beta-endorphin levels than did patients with symptomatic ischemia, especially during exercise. With naloxone treatment, the pain threshold of patients with silent myocardial ischemia (SMI) can be reduced to the same values as those of symptomatic patients. This supports the possibility of a role for endorphins in SMI. Patients who experience both asymptomatic and symptomatic ischemic episodes do so because their pain threshold and endorphin regulatory system varies throughout the day and because severity and duration of ischemic episodes are different. Although there is controversy over the appropriate therapy for SMI, it is more likely that this should simply be treated in the same way as painful ischemia.
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PMID:Silent myocardial ischemia. 268 1

30 males, suffering from ischemic heart disease (IHD), and stable exertional angina pectoris, whose age ranged from 60 to 74 years and also 15 apparently healthy volunteers of the same age participated in the study. The IHD patients' blood displayed increased basal levels of adrenocorticotropic hormone (ACTH), cortisol, and met-enkephalins. During graded physical exercise two types of hormonal system response were established: in the first group of patients the plasma ACTH and cortisol levels were seen to rise at maximal threshold load, while in the second group the content of the above hormones declined. The first group of patients showed a less economical hemodynamic response to standard loading in comparison to the second group. A relation was found between changes in hemodynamic system and function of pituitary-adrenal system in elderly IHD patients during physical exercise. Inadequate ACTH and cortisol increase in the course of effects of stress contributed to IHD aggravation in old age, along with reduced tolerance to physical exercise. beta-Adrenoblocker, propranolol, influenced both types of hormonal response, thereby diminishing their shifts in physical stress.
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PMID:Hormonal supply during physical exercise in elderly patients with ischemic heart disease. 283 99

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

Relief of discomfort during acute myocardial ischemia is usually accomplished with a narcotic analgesic. Because these medications may cause unpleasant symptoms and exert a possibly adverse hemodynamic effect, the availability of alternative analgesic medication would be advantageous. Nitrous oxide is a commonly used potent analgesic gas. Nitrous oxide has been used to relieve ischemic discomfort during myocardial infarction. The current study was undertaken to corroborate that data in a randomized, blinded, cross-over study and to begin to explore a mechanism for the analgesic effect. Twelve patients with typical ischemic chest discomfort and a suspected myocardial infarction were included in the study. Each patient received a 30-minute inhalation treatment of 30% nitrous oxide/70% oxygen and 30 minutes of 30% room air/70% oxygen. Patients were blinded to their treatment and were randomized to receive nitrous oxide first, then room air, or vice versa. A semiquantitative assessment of the severity of chest discomfort was made before, during, and at the conclusion of each treatment together with a measurement of plasma beta-endorphin levels using a venous blood sample. Eleven of the 12 patients reported a significant reduction in the intensity of their chest discomfort during the nitrous oxide inhalation, but none had pain relief during the control period. Beta-endorphin levels fell to a greater extent during the inhalation of nitrous oxide than during the control period (51% versus 26%; P less than .05). No significant adverse effects were noted and most patients slept during the nitrous oxide inhalation. It is concluded that nitrous oxide anesthesia is a superior method of pain relief in patients with ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrous oxide anesthesia in patients with ischemic chest discomfort: effect on beta-endorphins. 296 38

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

Although silent myocardial ischemia is a well recognized phenomenon, the reasons for the lack of symptoms in patients with coronary artery disease (CAD) is unclear. Because the endogenous opioid beta-endorphin has been related to pain modulation, plasma beta-endorphin levels were studied before, during and after exercise-induced ischemia in symptomatic and asymptomatic men. Because beta-endorphin responses have been closely linked to adrenocorticotropic hormone (ACTH) and cortisol responses, these hormones also were measured. Nine symptomatic and 12 asymptomatic patients with a high probability (at least 95%) of CAD and 8 apparently healthy men completed a Bruce protocol treadmill test. Blood samples were drawn before, during and 10 minutes after exercise. During exercise the measured hormones showed no significant increases from basal levels. However, plasma beta-endorphin, ACTH and cortisol levels were significantly elevated (p less than or equal to 0.01) 10 minutes after exercise in all 3 groups. There was no significant difference in plasma beta-endorphin levels during or after exercise between the symptomatic and asymptomatic patients with CAD. Thus, differences in circulating levels of beta-endorphin, ACTH and cortisol are not associated with the presence or absence of pain during exercise-induced myocardial ischemia.
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PMID:Plasma beta-endorphin levels in silent myocardial ischemia induced by exercise. 303 88

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

Plasma beta-endorphin levels were measured by radioimmunoassay before and after exercise in 25 patients with coronary artery disease. Eighteen patients were men and 7 were women; age range was 36 to 75 years (mean 60). All patients had angina pectoris, a positive treadmill test response or positive exercise radionuclide findings. The mean preexercise plasma endorphin level was 4.9 +/- 3.0 pmol/liter (range 0.7 to 13.5). The mean postexercise plasma endorphin level of 6.6 +/- 4.6 mol/liter (range 0 to 19.5) was significantly higher (p less than 0.05). A significant positive correlation was seen between postexercise endorphin levels and time to onset of angina (r = 0.4, p = 0.03). There were negative correlations between postexercise endorphin levels and occurrence (r = -0.4, p = 0.04) and duration of angina (r = -0.4, p = 0.05). No association was found for maximal heart rate-blood pressure product, workload, time to ST-segment depression or stress ejection fraction. A positive correlation was found between rest left ventricular ejection fraction and postexercise endorphin levels (r = 0.5, p = 0.02). In conclusion, in patients with exercise-induced myocardial ischemia, plasma beta-endorphin levels are increased after exercise; postexercise endorphin levels are related to timing and occurrence (presence or absence) of angina; and endorphins may alter the perception of pain caused by myocardial ischemia.
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PMID:Endorphins are related to pain perception in coronary artery disease. 382 89


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