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)

To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive beta-endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF beta-endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.
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PMID:CSF beta-endorphin and leu-enkephalin levels in the acute and chronic stages of cerebral infarction. 295 70

Naloxone has been reported to have potential benefit in the treatment of stroke. We evaluated the effect of naloxone in a double-blind trial conducted with 15 stroke patients whose deficits ranged from 8 to 60 hours in duration. All but one patient sustained a cerebral infarction. Neurologic function was assessed before and five minutes after each of two injections given to each patient in a double-blind fashion. The injections consisted of naloxone (0.4 mg in 3 patients and 4.0 mg in 12 patients) and saline. Prior to the trial, samples of plasma were obtained for determination of immunoreactive beta-endorphin for each patient. Four patients showed minimal improvement following injection of naloxone, while five patients exhibited a slightly greater improvement following saline injection. There were no significant elevations of plasma beta-endorphin among stroke patients. We conclude that naloxone may not have a significant therapeutic role for stroke in the clinical setting.
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PMID:A double blind trial of naloxone in the treatment of acute stroke. 608

beta-Endorphin was measured in cerebrospinal fluid (CSF) and plasma in patients with cerebral infarction at acute (4 to 48 hours) and chronic (1 month) stages. Only CSF samples obtained in the acute stage showed beta-endorphin values that were statistically higher than those measured in a control population. This finding suggests that infarction at its acute stage gives rise to an increased release of beta-endorphin. Such a mechanism is consistent with the possibility that the reported therapeutic effect of naloxone in cerebral ischemic lesions may result in part from the antagonism of the centrally released endorphin, beta-endorphin.
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PMID:Increase of beta-endorphin levels in cerebrospinal fluid but not in plasma in patients with cerebral infarction. 608 32