Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
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.
 ...
PMID:[Blood endorphin levels in myocardial infarction]. 244 22

An improved radio-immunoassay using an antiserum directed towards the N-terminal part of the endogenous opioid peptide beta-endorphin 1-31 (beta-EP) was validated and applied to a study of beta-EP in plasma during ischaemic pain. Experimental ischaemic pain induced in seven healthy volunteers by the submaximal effort tourniquet test did not change plasma beta-EP or adrenocorticotrophin. Plasma beta-EP was determined in 21 patients with acute myocardial infarction (AMI) and in seven patients with unstable angina pectoris. Plasma beta-EP was 4.9 fmol/ml with 95% confidence limits, 3.2-7.8 fmol/ml in AMI patients at admittance, and 2.9 (2.0-3.4) fmol/ml one week later in stable and pain-free condition (p less than 0.05). The level in 49 healthy persons was 2.8 (2.4-2.9) fmol/ml. Elevated beta-EP levels were found in five AMI patients with cardiogenic shock and in four AMI patients dying within 24 h after admittance compared to the rest of AMI patients (p less than 0.02). beta-EP was not elevated during unstable angina pectoris, although pain scores were similar to AMI. The AMI group revealed a significant, although weak, positive correlation between plasma beta-EP and pain score (Spearman r = 0.49, p less than 0.05), while there was no correlation during unstable angina pectoris. beta-EP was not correlated to the amount of morphine required within the 48 h after admittance of AMI patients. We conclude that the increase of beta-EP in plasma during AMI may be due to stressful factors other than ischaemic pain and that it is questionable whether beta-EP in plasma is related to antinociception.
 ...
PMID:Plasma beta-endorphin during clinical and experimental ischaemic pain. 296 68

Adrenocortical function, as reflected by sequential analysis of plasma cortisol and adrenocorticotropin (ACTH) test, was investigated in elderly patients (greater than or equal to 65 years) with acute myocardial infarction (AMI), and compared to young patients (less than or equal to 55 years) with AMI. Further, age-matched subjects admitted with ischaemic chest pain, in whom AMI was not verified, served as controls. Following infarction, plasma cortisol peaked within 24 hours in both age groups, whereupon the cortisol level gradually decreased till day 12. Plasma cortisol during AMI disclosed no age-related difference, but was significantly correlated to the localization of infarction and lactate dehydrogenase (LDH). The development of complications, i.e. hypotension, congestive heart failure, and arrhythmia, calling for therapeutic intervention, was solely correlated to infarct size, as estimated by peak LDH. Young and elderly patients responded equally and normally to ACTH stimulation, and in both groups a significant, positive correlation between the basal and the 30-min plasma cortisol was observed. Thus, we may conclude that in patients with AMI, the hypothalamic-pituitary-adrenocortical (HPA) response to stress and ACTH test shows no repression due to age.
 ...
PMID:Adrenocortical function in old age as reflected by plasma cortisol and ACTH test during the course of acute myocardial infarction. 322 33

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.
 ...
PMID:Silent ischaemia in post-myocardial infarction patients submitted to physical training. 324 37

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.
 ...
PMID:Plasma levels of endogenous opioid peptides in patients with acute myocardial infarction. 747 58

We tested the idea that cytokine antagonists are released during acute myocardial ischemia to counteract proinflammatory effects of cytokines. We investigated changes in plasma concentrations of the anticytokine molecules alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) in patients with acute myocardial infarction (AMI) or unstable angina (UA). Blood samples were collected at presentation in the coronary care unit, at 3-hour intervals for 24 hours, and daily for 4 days thereafter. There were no significant differences in the concentrations of cytokine antagonists in patients with AMI or UA. However, whereas concentrations of alpha-MSH were increased in early samples of patients with AMI or UA who were treated with a thrombolytic agent, they were consistently low in untreated patients. IL-1ra concentrations likewise were greater 3 and 6 hours after treatment in patients who underwent thrombolysis, whereas there was no significant difference in plasma sTNFr between the two groups. We suggest that during myocardial ischemia and thrombolysis anticytokine molecules released from the injured myocardium become available to reduce inflammation caused by cytokines and other mediators of inflammation.
 ...
PMID:Endogenous cytokine antagonists during myocardial ischemia and thrombolytic therapy. 763 97

We measured plasma concentration of alpha-melanocyte-stimulating hormone (alpha-MSH), a proopiomelanocortin derivative that modulates pyrogenic and proinflammatory effects of cytokines, in infectious and inflammatory disorders in humans to learn if changes in this peptide take place in naturally occurring disease. alpha-MSH was elevated in HIV-infected patients of the CDC groups III and IV. Although the peptide increased in the circulation of normal subjects injected with endotoxin, it was reduced in patients with septic syndrome. alpha-MSH was found in the synovial fluid of arthritis patients, and its concentration was greater in the forms of arthritis marked by greater inflammation. We found that alpha-MSH is increased in the circulation of patients with acute myocardial infarction receiving thrombolytic therapy. Plasma concentrations of alpha-MSH is increased in the circulation of patients with acute myocardial infarction receiving thrombolytic therapy. Plasma concentrations of alpha-MSH were lower in healthy elderly subjects than in young controls. Because an excess of proinflammatory cytokines can have detrimental effects, we investigated the influences of alpha-MSH on the production of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in HIV-infected patients and in patients with septic syndrome. Production of these cytokines in whole-blood samples stimulated with endotoxin was significantly reduced by treatment of blood with alpha-MSH. alpha-MSH has been injected into at least 106 human subjects to study its effects on pituitary function, menstrual bleeding, and tanning. The peptide was always well tolerated. alpha-MSH administration could open new perspectives in treatment of inflammatory diseases in humans.
 ...
PMID:The neuropeptide alpha-MSH in HIV infection and other disorders in humans. 962 10

Lymphocytes can be activated to produce and release opioid peptides. We investigated the levels of immunoreactive beta-endorphin in peripheral blood mononuclear cells from 11 patients with acute myocardial infarction. The concentrations of beta-endorphin in mononuclear leukocytes of 30.2 +/- 6.9 pg/10(6) cells on admission were in the normal range of 20-40 pg/10(6) cells and decreased significantly to 6.9 +/- 1.9 pg/10(6) cells after 48 h (p < 0.05). Decreased levels of mononuclear leukocyte-associated beta-endorphin in acute myocardial infarction may be due to the release of endogenous opioid after stimulation by stress and acute-phase reactants and play a role in inflammation and pain.
 ...
PMID:Decreased levels of beta-endorphin in circulating mononuclear leukocytes from patients with acute myocardial infarction. 969 70

A 59-year-old man with a 30-year history of type 2 diabetes mellitus presented with fatigue, confusion, and weight loss over a 3-month period. He was found to be hypercalcemic (11.8 mg/dL) and dehydrated, and his hypercalcemia improved with intravenous fluids. While in the hospital, he developed hyponatremia, hypoglycemia, and hypotension. He was found to have a subnormal cortisol level of 2.3 microg/dL at baseline, which increased to only 5.6 microg/dL 60 minutes after a 250-microg corticotropin intravenous stimulation test. The patient developed pneumonia and adult respiratory distress syndrome and died of an acute myocardial infarction. During the autopsy, he was found to have lymphocytic hypophysitis with a severe reduction in corticotropin-producing anterior pituitary cells. No malignancy was identified at autopsy. He is the first male patient to be described in the literature who presented with hypercalcemia caused by lymphocytic hypophysitis.
 ...
PMID:Lymphocytic hypophysitis in a man presenting with hypercalcemia. 1126


1 2 Next >>