Beta-Endorphin Response to an Acute Pain Stimulus
Male; Pain Measurement; Time Factors; Reproducibility of Results; Animals; Mice; Acute Disease; Biomarkers of Pain; Physical Stimulation; Animal; beta-Endorphin/analysis/metabolism/secretion; Biological Markers/analysis/blood; Disease Models; Inbred DBA; Neurochemistry/methods; Pain/blood/physiopathology; Radioimmunoassay/methods; Up-Regulation/physiology
The timing of the measurement of biological samples (e.g. biomarkers) is not always standardized. Biomarkers are the focus of many recent studies and treatments. The purpose of this study was to determine the timing of the release of beta-endorphin (BE), a possible biomarker, after exposure to pain and/or handling stress in order to standardize measurements. Mouse plasma was collected for BE analysis following handling i.e. being picked up by the investigator, exposure to a painful (55 degrees C hot-plate), or exposure to a nonpainful stimulus (room temperature hot-plate). The groups exposed to either a painful or nonpainful stimulus released BE in response to the stimulus, but the duration of the response was longer in mice exposed to a painful stimulus than in mice exposed to a nonpainful stimulus. The BE in the mice exposed to a nonpainful stimulus peaked at 1 min and returned to baseline levels by 5 min while the BE response of the mice exposed to a painful stimulus peaked at 10 min and remained elevated for 25 min. The results of this study indicate that BE can be a biomarker for pain and handling stress, however, the timing of the measurement should differ.
Rasmussen NA; Farr LA
Journal Of Neuroscience Methods
2009
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/j.jneumeth.2008.10.013" target="_blank" rel="noreferrer noopener">10.1016/j.jneumeth.2008.10.013</a>
Plasma beta-endorphin during clinical and experimental ischaemic pain
Female; Humans; Male; Adult; Aged; Middle Aged; beta-Endorphin/blood; Biomarkers of Pain; Radioimmunoassay/methods; Angina Pectoris/blood; Blood Specimen Collection; Exertion; Muscles/physiology; Myocardial Infarction/blood; Pain/blood/etiology; Tourniquets
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.
1987
Bach FW; Fahrenkrug J; Jensen K; Dahlstrom G; Ekman R
Scandinavian Journal Of Clinical And Laboratory Investigation
1987
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1080/00365518709168942" target="_blank" rel="noreferrer">10.1080/00365518709168942</a>
Novel opioid peptides endomorphin-1 and endomorphin-2 are present in mammalian immune tissues
Female; Humans; Male; Adult; Middle Aged; Animals; Rats; Non-U.S. Gov't; Research Support; Wistar; Radioimmunoassay/methods; Chromatography; High Pressure Liquid; Oligopeptides/analysis; Cross Reactions; Immune Sera/immunology; Immune System/chemistry; Spleen/chemistry; Thymus Gland/chemistry; Tissue Extracts/chemistry
Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides, reported within the central nervous system, which have very high specificity and affinity for the mu-opioid receptor. We have used newly developed and well-characterised radioimmunoassays (RIAs) in combination with reversed-phase high-performance liquid chromatography (HPLC) to detect EM-1 and EM-2 immunoreactivity (ir) in rat immune tissues. Endomorphins were detectable in extracts of rat spleen (total EM-1-ir/spleen: 440+/-73 pg, mean+/-SEM, a=group of eight rats; EM-2-ir: 150+/-12 pg) and thymus (EM-1-ir: 152+/-18 pg, mean+/-SEM n=8; EM-2-ir: 156+/-28 pg). EM-2-ir was detectable in extracts of human spleen (338+/-196 pg/g tissue, n=3). Multiple peaks of EM-1-ir and EM-2-ir were observed in rat spleen and thymus extracts, and multiple peaks of EM-2-ir were observed in extracts of human spleen, following reversed-phase HPLC and RIAs. This is the first report of endomorphin immunoreactivity in tissues of the rat and human immune systems.
2000
Jessop DS; Major GN; Coventry TL; Kaye SJ; Fulford AJ; Harbuz MS; De Bree FM
Journal Of Neuroimmunology
2000
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1016/s0165-5728(99)00216-7" target="_blank" rel="noreferrer">10.1016/s0165-5728(99)00216-7</a>