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Mediators of Inflammation
Volume 2013, Article ID 627831, 7 pages
Research Article

Dexmedetomidine Reduced Cytokine Release during Postpartum Bleeding-Induced Multiple Organ Dysfunction Syndrome in Rats

1Department of Anesthesiology, Third Affiliated Hospital, Guangzhou Medical University, Guangzhou 510150, China
2Department of Pathology, Detroit Medical Center, Harper University Hospital, School of Medicine, Wayne State University, 3990 John R, Detroit, MI 48201, USA
3Department of Gynecology and Obstetrics, Third Affiliated Hospital, Guangzhou Medical University, Guangzhou 510150, China

Received 25 June 2012; Revised 7 March 2013; Accepted 22 May 2013

Academic Editor: Celeste C. Finnerty

Copyright © 2013 Liu Xianbao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Dexmedetomidine (DEX) is an α2-adrenergic agonist. It decreases the levels of norepinephrine release, resulting in a reduction of postsynaptic adrenergic activity. In the present study, the effects of DEX on postpartum bleeding-induced multiple organ dysfunction syndrome (BMODS) were studied in rats in which BMODS was induced by the combination of hypotension and clamping of the superior mesenteric artery. We evaluated the role of dexmedetomidine (DEX) in cytokine release during postpartum BMODS in rats. In summary, the present study demonstrated that DEX administration reduced IFN-r and IL-4 release and decreased lung injury during postpartum BMODS. It is possible that DEX administration decreased inflammatory cytokine production in BMODS by inhibiting inflammation and free radical release by leukocytes independent of the DEX dose.