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      Decreased Levels of β-Endorphin in Circulating Mononuclear Leukocytes from Patients with Acute Myocardial Infarction

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          Lymphocytes can be activated to produce and release opioid peptides. We investigated the levels of immunoreactive β-endorphin in peripheral blood mononuclear cells from 11 patients with acute myocardial infarction. The concentrations of β-endorphin in mononuclear leukocytes of 30.2 ± 6.9 pg/10<sup>6</sup> cells on admission were in the normal range of 20–40 pg/10<sup>6</sup> cells and decreased significantly to 6.9 ± 1.9 pg/10<sup>6</sup> cells after 48 h (p < 0.05). Decreased levels of mononuclear leukocyte-associated β-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.

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          Most cited references 11

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          Inflammation and coronary artery disease.

           R. Alexander (1994)
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            Peripheral mechanisms of opioid antinociception in inflammation: involvement of cytokines.

            It has been shown previously that opioids induce antinociceptive effects at peripheral sites in the presence of inflammatory processes. Besides being elicited by local injection of opioids, such effects can also be obtained by activation of intrinsic opioid mechanisms, e.g. following stress. In the present study the possible role of cytokines in this mechanism was investigated. Unilateral inflammation of the hindpaw of rats was induced by local injection of Freund's complete adjuvant. Intraplantar injection of tumor necrosis factor alpha (TNF alpha) or interleukin-6 induced a dose-dependent increase in the threshold in the paw pressure test in the inflamed but not in the non-inflamed paw. This increase was prevented by local injection of naloxone and the mu-opioid receptor specific antagonist CTOP (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2) as well as by 3-E7, an universal opioid peptide antibody. In rats pretreated with cyclosporin A to suppress the immune system, the antinociceptive effect of TNF alpha was completely inhibited. In concert with previous studies these data indicate that the tested cytokines release opioid peptides (e.g. beta-endorphin and/or enkephalins) from immune cells of the inflamed tissue which act on opioid receptors present on sensory nerve terminals, resulting in antinociception.
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              Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease.

              Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.

                Author and article information

                S. Karger AG
                July 1998
                14 August 1998
                : 90
                : 1
                : 43-47
                a Intensive Care Unit, Department of Medicine, University of Innsbruck, Austria; b Department of Pharmacology, University of Milan, Italy
                6815 Cardiology 1998;90:43–47
                © 1998 S. Karger AG, Basel

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                Page count
                Pages: 5
                Coronary Care


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