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pubmed-article:17996950pubmed:abstractTextMice were exposed to restraint stress for 3h. During this period, low body temperature (hypothermia, 39 degrees C-->less than 37 degrees C) and high blood glucose levels (hyperglycemia, 150 mg/dl-->up to 220 mg/dl) were simultaneously induced. Reflecting a stress-induced phenomenon, blood levels of catecholamines increased at that time. Administration of adrenaline (alpha-stimulus), but neither noradrenaline (alpha but less than adrenaline) nor isoproterenol (beta), induced a similar stress-induced pattern of body temperature and blood glucose variations. This alpha-adrenergic effect was confirmed using alpha- and beta-blockers in adrenaline-induced hypothermia and hyperglycemia. By applying this alpha-stimulus, the effect on immunoparameters was then investigated. Stress-resistant lymphocyte populations were found to be NK cells, extrathymic T cells and NKT cells, especially in the liver. Functional assays showed that both NK-cell cytotoxicity and NKT-cell cytotoxicity were augmented by alpha-stimulus. These results suggest that alpha-stimulus is one of the important factors in the stress-induced phenomenon and that it eventually produces hypothermia, hyperglycemia and innate-immunity activation seen during stress.lld:pubmed
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pubmed-article:17996950pubmed:pagination43-9lld:pubmed
pubmed-article:17996950pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:17996950pubmed:articleTitleRole of alpha-adrenergic stimulus in stress-induced modulation of body temperature, blood glucose and innate immunity.lld:pubmed
pubmed-article:17996950pubmed:affiliationDepartment of Immunology, Niigata University School of Medicine, Niigata, Japan.lld:pubmed
pubmed-article:17996950pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17996950pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed