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  • Title: [Beta-endorphin in acute focal cerebral infarct].
    Author: Marín Gámez N, Bermúdez García JM, Aguilar Martínez JL, Ruiz Requena ME, Raya Muñoz J, del Arbol JL.
    Journal: Med Clin (Barc); 1989 Sep 16; 93(7):252-5. PubMed ID: 2554075.
    Abstract:
    Experimental studies in animal models suggest that the endorphin system may be implicated in the pathogenetic mechanism of cerebral ischemic lesions. Naloxone has been shown to possess a beneficial effect on the neurologic deficit associated with cerebral ischemia in animal experiments, probably because of its endorphin antagonist properties. By contrast, the results of clinical trials are contradictory. Moreover, the true significance of high plasma levels of beta-endorphin in patients with acute focal cerebral infarct (AFCI) has not yet been elucidated. We have evaluated 23 patients with established AFCI, in whom plasma levels of beta-endorphin and corticotropin (ACTH) were simultaneously measured during the first 48 hours after the onset of the disease. The results were compared with those from a control group. In a subgroup of 9 cases new measurements were made after 7 days. In the patients with AFCI, significantly lower levels of beta-endorphin and ACTH than in the control group were found. One week later, a moderate nonsignificant increase in the plasma level of beta-endorphin was found. The localization and estimated size of the infarct area were not relevant. Probably, the plasma levels of beta-endorphin will need to be considered before naloxone therapy is indicated, and only if it is confirmed that the plasma levels of beta-endorphin reflect changes at the cerebral level, as the pathophysiological role of these opioids in AFCI has not yet been established.
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