l-663536 and Hypothermia

l-663536 has been researched along with Hypothermia* in 2 studies

Other Studies

2 other study(ies) available for l-663536 and Hypothermia

ArticleYear
Involvement of eicosanoids in the hypothermic response to lipopolysaccharide during endotoxemia in rats.
    Prostaglandins, leukotrienes, and essential fatty acids, 2004, Volume: 70, Issue:1

    Hypothermia is one of the prominent features of the acute phase response to endotoxin (LPS). This study was undertaken to elucidate the effects of the COX-inhibitor Indomethacin (INDO) and the selective FLAP inhibitor MK-886 on LPS-induced hypothermia, mortality and increase in production of hypothalamic prostaglandin E(2) (PGE(2)) and leukotriene during endotoxemia. It has been demonstrated that INDO and MK-886 significantly attenuate the hypothermia induced by LPS, but MK-886 has a lesser (protective) effect than INDO. Only INDO was found to attenuate significantly the hyperthermic response to LPS. Furthermore, INDO significantly reduced the elevation in hypothalamic PGE(2) levels. MK-886 significantly reduced the elevation in hypothalamic leukotriene production only when LPS was given in a dose of 1mg/kg. Both drugs failed to reduce the elevation in plasma TNF-alpha and mortality induced by LPS. We conclude that in rats, febrile response to endotoxin involves many inflammatory mediators. However, it seems that PGE(2) and leukotrienes do not have a pivotal role in the mechanism of LPS-induced mortality.

    Topics: Animals; Body Temperature; Dose-Response Relationship, Drug; Eicosanoids; Endotoxemia; Fever; Hypothermia; Indoles; Indomethacin; Lipopolysaccharides; Male; Rats; Rats, Sprague-Dawley; Survival Rate; Time Factors; Tumor Necrosis Factor-alpha

2004
Evidence supporting involvement of leukotrienes in LPS-induced hypothermia in mice.
    The American journal of physiology, 1999, Volume: 276, Issue:1

    The aim of the present study was to examine a possible involvement of leukotrienes (LTs) in lipopolysaccharide (LPS)-induced body temperature (Tb) response. We examined the effect of MK-886, an inhibitor of LT synthesis, on changes in Tb, plasma tumor necrosis factor-alpha (TNF-alpha), hypothalamic LT, and PGE2 production. Intraperitoneal injection of LPS (50 microgramg/mouse) led to a decrease in Tb starting 1 h after the injection. The hypothermic effect of LPS was accompanied by a significant elevation in TNF-alpha level in plasma and in LT and PGE2 production by ex vivo-incubated hypothalamus. MK-886 (1 mg/kg ip) administered 4 h before LPS efficaciously prevented LPS-induced hypothermia in mice. Pretreatment of mice with MK-886 did not alter the LPS-stimulated increase in plasma TNF-alpha. MK-886 significantly inhibited LT and enhanced PGE2 production in hypothalamus compared with LPS alone. These results suggest that 1) LPS-induced hypothermia may be mediated by LTs and 2) the antihypothermic effect of MK-886 is not associated with TNF-alpha bioactivity.

    Topics: Animals; Body Temperature; Dinoprostone; Hypothalamus; Hypothermia; Indoles; Leukotrienes; Lipopolysaccharides; Lipoxygenase Inhibitors; Male; Mice; Mice, Inbred Strains; Tumor Necrosis Factor-alpha

1999