beta2-Adrenoceptor blockade partially restores ex vivo TNF production following hemorrhagic shock.
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| Abstract |
The aim of the study was to assess the mechanisms through which leukocyte deactivation occurs upon hemorrhagic shock. In particular, the influence of beta-adrenergic tone was evaluated. BALB/c mice were hemorrhaged and resuscitated 60 min after hemorrhage. Animals were sacrificed 60 min later by exsanguination. Blood from exsanguination was cultured ex vivo with lipopolysaccharide (LPS) and heat-killed Staphylococcus aureus Cowan I (SAC). Hemorrhage resulted in a major decrease of LPS-induced TNF production whereas IL-10 production was significantly enhanced. Selective beta(2)-adrenoceptor antagonists (ICI 118,551) attenuated the decrease in TNF production and further enhanced IL-10 production. Hemorrhage did not alter SAC-induced TNF production levels whereas IL-10 production was increased. ICI 118,551 further increased the production of both TNF and IL-10. These data suggest that leukocyte deactivation after LPS stimulation is not a generalized phenomenon since TNF production was maintained when another microbial activator was used. IL-10 production was enhanced after hemorrhagic shock, independently of the nature of the triggering agent. Finally, this study demonstrates that beta(2)-adrenoceptor ligands play an important role in blood leukocyte deactivation to LPS after hemorrhagic shock.
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| Authors | Karim Asehnoune, Catherine Fitting, Alain R Edouard, Vincent Minville, Dan Benhamou, Jean-Marc Cavaillon, Pierre Moine |
| Journal | Cytokine (Cytokine) Vol. 34 Issue 3-4 Pg. 212-8 (May 2006) ISSN: 1043-4666 [Print] England |
| PMID | 16790355 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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