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Nitric Oxide Regulates Prostaglandin E2 Release by Rat Kupffer Cells

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Host Defense Dysfunction in Trauma, Shock and Sepsis

Abstract

Nitric oxide has recently been identified as an intermediate of mammalian nitrogen metabolism [1, 2]. This highly reactive radical is derived from the amino acid L-arginine and degrades within seconds into its stable end products nitrite and nitrate. Important biological functions of nitric oxide include regulation of vascular tone [1], inhibition of thrombocyte adherence and aggregation [3], as well as enhancement of macrophage cytotoxicity [4]. Macrophage nitric oxide biosynthesis is inducible, namely by inflammatory mediators such as lipopolysaccharide (LPS) [5]. Kupffer cells, the fixed macrophages of the liver, also produce nitric oxide in response to LPS [6]. In addition, LPS-stimulated Kupffer cells release cytokines, which induce nitric oxide synthesis in hepatocytes [7]. The role of nitric oxide in the septic liver is not very well understood. Experiments were undertaken to determine whether nitric oxide synthesis influences other functions of Kupffer cells, specifically the release of eicosanoids.

This work was supported by National Institutes of Health grants GM 44100 (T.R.B.) and GM 37753 (R.L.S.) J. S. was supported by a fellowship of the Deutsche Forschungs gemeinschaft, Bonn Germany (Sta 311/1-1).

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© 1993 Springer-Verlag, Berlin Heidelberg

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Stadler, J. et al. (1993). Nitric Oxide Regulates Prostaglandin E2 Release by Rat Kupffer Cells. In: Faist, E., Meakins, J.L., Schildberg, F.W. (eds) Host Defense Dysfunction in Trauma, Shock and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77405-8_63

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  • DOI: https://doi.org/10.1007/978-3-642-77405-8_63

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-77407-2

  • Online ISBN: 978-3-642-77405-8

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