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 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.
 ...
PMID:Endorphins are related to pain perception in coronary artery disease. 382 89

Whether i.v. infusion of beta-endorphin or metenkephalin can modify adenosine-provoked angina pectoris-like pain was investigated in healthy volunteers with a double-blind controlled design. All seven volunteers experienced dose-related adenosine-provoked chest pain. Metenkephalin did not modulate the dose-effect curve for adenosine while beta-endorphin counteracted (p < 0.01) the development of pain. The results suggest that peripheral p.subtype opioid receptors are involved in the modulation and may play a role in the genesis of silent and painful myocardial ischaemia.
 ...
PMID:Beta-endorphin but not metenkephalin counteracts adenosine-provoked angina pectoris-like pain. 890 8

Earlier studies have shown that spinal cord stimulation (SCS) has antianginal and anti-ischemic effects in severe coronary artery disease. In the present study, 14 patients were subjected to right-sided atrial catheterization and atrial pacing. The patients were paced to angina during a control session and during spinal cord stimulation. Myocardial extraction of beta-endorphin (BE) during control pacing (8 +/- 22%) changed to release at the maximum pacing rate during treatment (-21 +/- 47%, a negative value representing release). Furthermore, the results indicate local myocardial turnover of leuenkephalin, BE and calcitonin-gene-related peptide. In addition, it is implied that SCS may induce myocardial release of BE which could explain the beneficial effects in myocardial ischemia.
 ...
PMID:Myocardial turnover of endogenous opioids and calcitonin-gene-related peptide in the human heart and the effects of spinal cord stimulation on pacing-induced angina pectoris. 977 55

We report a 62-year-old male patient who had variant angina and isolated adrenocorticotropic hormone (ACTH) deficiency. His serum sodium concentration was low and vasopressin was inappropriately high for the low plasma osmolality. Serum free thyroxine (FT4) was low and thyroid stimulating hormone (TSH) was high with positive anti-thyroperoxidase antibodies, compatible with Hashimoto's thyroiditis. Treatment with Amrodipine and hydrocortisone relieved chest symptoms and hyponatremia, and hypothyroidism was also normalized. It is suggested that coronary artery spasm may be related to cortisol deficiency and/or inappropriately high vasopressin secretion and that hypothyroidism was ameliorated because the reduced responsiveness to TSH returned to normal due to hydrocortisone supplement.
 ...
PMID:Variant angina in isolated adrenocorticotropin deficiency, inappropriate vasopressin secretion and Hashimoto's thyroiditis. 963 Feb 2

Nowadays the cardiovascular diseases particularly ischaemic heart disease (IHD) are the most frequent causes of death in Poland. Some of patients with IHD are completely asymptomatic. These subjects are more susceptible to sudden coronary events due to lack of diagnosis and treatment. Cohn divided patients with asymptomatic ischaemia (AI) into three groups: completely asymptomatic, asymptomatic patients after myocardial infarction, patients with painful angina who have some ischaemic events asymptomatic. Some causes of AI are: increased pain threshold, increased beta-endorphin levels, impairment of pain pathways, smaller ischaemic regions in comparison with painful angina, psychological factors, transient platelet microaggregates. Estimated prevalence of AI is about 2-4% of total population and is larger in the group of patients with multiple coronary disease risk factors especially with diabetes mellitus (autonomic neuropathy). In the patients after myocardial infarction the prevalence of AI is between 30-70% and it is associated with poorer prognosis. In subjects with painful angina 70-80% of total ischaemic episodes detected by 24-hour ECG monitoring is asymptomatic. The most useful methods for diagnosis of AI are ECG exercise test and ambulatory 24-hour ECG monitoring, although they may sometimes produce false positive results. Other tests are not widely performed and their use is restricted to specific circumstances. Some cases are finally solved by coronary angiography. Although screening in whole population is not cost-effective, but in some groups is necessary (people with many risk factors of IHD, people of certain professions--plane pilots, etc.). Treatment of AI does not vary from treatment of symptomatic IHD. Basic drugs used are: aspirin, beta-blockers, calcium channel blockers, long time acting nitrates. Positive effect of statins is also observed. The most beneficial is invasive treatment--CABG is more efficient than PTCA. Moreover the treatment of symptomatic IHD should be oriented not only to eliminate the symptoms but also to withdraw episodes of silent ischaemia confirmed by 24-h ECG monitoring or ECG exercise test.
 ...
PMID:[Silent myocardial ischemia]. 1147 58


<< Previous 1 2 3