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

Plasma levels of beta-endorphin, met-enkephalin and dynorphin were assessed in acute myocardial infarction (AMI) patients, with and without pain (group I: no pain, N = 12; group II: severe pain, N = 16). Plasma opioid peptide concentration was measured on admission to hospital (between 1 and 3 h after the myocardial infarction onset), at 7, 12, 24 h and at 2, 3 and 4 days. A transient increase in plasma beta-endorphin levels was found in AMI patients with severe pain, the levels normalizing within 12-18 h when pain had ceased. No changes in beta-endorphin concentration were observed in AMI patients without pain. Compared with healthy subjects, low levels of met-enkephalin were found in both groups of AMI patients throughout the study. Low levels of dynorphin were observed in patients with no pain while in the other patients initial low levels of dynorphin normalized when pain ceased. Blood pressure, heart rate and central venous pressure values were normal and did not correlate with plasma opioid levels. The results suggest that endogenous opioids do not affect pain in the early phase of myocardial infarction. The rise in beta-endorphin concentration observed in patients with severe pain seems to be induced by pain stress.
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PMID:Plasma endogenous opioid levels in acute myocardial infarction patients, with and without pain. 135 15

Blood gamma-endorphin concentrations were repeatedly measured, using an original radioimmunoassay, in patients with myocardial infarction. In the early days of acute myocardial infarction, high levels of this opioid peptide were observed, then plasma gamma-endorphin concentration gradually decreased by the time of discharge. In patients with grave complications, gamma-endorphin level was significantly lower, as compared to patients with uncomplicated infarction.
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PMID:[Blood endorphin levels in myocardial infarction]. 244 22

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

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

The effect of opiate peptides (leu-enkephalin, met-enkephalin and beta-endorphin) as well as of enkephalin synthetic analogs (two tetrapeptides and dalargin hexapeptide) on the activity of blood enzymes CPK and LDG1, the scope of myocardial infarction and ultrastructure of periinfarction cardiomyocytes has been studied on 200 white outbred rats with simulated myocardial infarction. The endogenous opiate peptides and dalargin hexapeptide were found to significantly decrease CPK and LDG1 activity and to diminish the size of the infarction. The effect is related to the drugs influence on the survival of periinfarction cardiomyocytes that can be proved electron-microscopically and using colloid lanthanum test.
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PMID:[Changes in the biochemical and morphological indices of structural disturbance in the peri-infarct area of the myocardium as affected by opioid peptides in an experiment]. 337 7

The effect of intravenous administration of the opioid antagonist naloxone in rats with acute left coronary artery ligation was studied. The results demonstrated that naloxone in a dose 2 mg/kg b. w. affords its protection on infarcted animals by two mechanisms: Reduces by 22% the incidence of early arrhythmias that occur within 15-20 minutes of acute myocardial ischaemia, and are responsible for the early (up to the 30th minutes) postligation death; Reverses the hypotension that results from the development of cardiogenic shock after 30 minutes myocardial infarction. The total mortality after naloxone treatment was significantly reduced by 22%. Naloxone does not influence significantly the size of the infarcted area but the incidence of left ventricle wall perforations was decreased by 38%. Both effects of naloxone are attributed to the antagonism of opioid receptors either directly on the myocardium or through blocking the central action of beta-endorphin. A direct effect of naloxone on the cardiac muscle action potential cannot be excluded.
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PMID:Opioid peptides in experimental myocardial infarction. I. The effect of naloxone. 361 53

Preliminary adaptation to brief immobilization stresses was shown to reduce impairments of the contractile function of the left ventricle in an experimental myocardial infarction both under conditions of physiological rest and following the short blocking of the aorta. This protective effect is occasioned, along with other factors, by the prevention of the stressory damage to the non-ischemic portions of the heart. The same adaptation increased the levels of enkephalins and beta-endorphin in the cerebral and adrenal structures. The preliminary administration of beta-endorphin prior to the stimulation of an experimental infarction considerably prevented stressory disorders of the contractile function of the right atrium.
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PMID:[Prevention of heart contractile disorders in experimental infarct by using preliminary adaptation to stress exposure and opioid peptides]. 654 54

There is substantial evidence that cardiac opioid receptors are activated during arrhythmias induced by administration of opioid peptides or myocardial ischemia, supporting the hypothesis that endogenous opioid peptides (EOP) are involved in myocardial infarction. This prospective clinical trial is designed to determine whether the ischemia-induced arrhythmias and extent of the infarct are related to the release of the EOP beta-endorphin in patients with acute myocardial infarction. Two groups were included in the study, patients with acute myocardial infarction, and healthy volunteers who served as controls. The results indicate that, compared to the controls, there was augmentation of ischemic arrhythmias and ischemic damage as assessed by serum creatine kinase activity, accompanied by an elevated level of beta-endorphin, in patients with acute myocardial infarction. The above data strongly indicate that EOP are indeed involved in the pathophysiology of myocardial infarction, and suggest these peptides have an important role in ischemic heart disease.
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PMID:Plasma levels of endogenous opioid peptides in patients with acute myocardial infarction. 747 58

Plasma beta-endorphin levels were estimated in patients with painless myocardial ischaemia. The survey was made in 90 patients with coronary artery disease: 55 of them after myocardial infarction and 35 with chronic stable angina pectoris. The control group comprised 22 healthy persons. Plasma beta-endorphin level was determined in all examined patients immediately before the exercise test, just after finishing exercise test, and 6 minutes after the termination of the exercise test. Beta-endorphin plasma levels has been determined with a radioimmunologic method by the means of "beta-endorphins [125J]RIA Kit" manufactured in NEN Research Products. Study showed that in the patients with silent myocardial ischaemia plasma beta-endorphin level was higher than in patients with painful myocardial ischaemia both at rest during exercise test. Increase of plasma beta-endorphin in examined patients can be one of etiopathogenetic factors of silent myocardial ischaemia.
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PMID:[Levels of B-endorphin in patients with silent myocardial ischemia]. 797 65


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