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Different cellular responses of dexmedetomidine at infected site and peripheral blood of emdotoxemic BALB/c mice
Authors:Rick Sai‐Chuen Wu  King‐Chuen Wu  Chiu‐Chen Huang  Yi‐Ying Chiang  Chia‐Chen Chen  Ching‐Lung Liao  Chin‐Nan Chu  Jing‐Gung Chung
Institution:1. Department of Anesthesiology, China Medical University Hospital, Taichung, Taiwan, Republic of China;2. Department of Anesthesia, E‐da Hospital / I‐Shou University, Kaohsiung, Taiwan, Republic of China;3. Graduate Institute of Chinese Medicine, China Medical University, Taichung, Taiwan;4. Department of Radiation Oncology, China Medical University Hospital, Taichung, Taiwan, Republic of China;5. Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, Republic of China;6. Department of Biotechnology, Asia University, Taichung, Taiwan, Republic of China
Abstract:Various sedative agents, including dexmedetomidine (dex), induce immunosuppression, and enhance infection progression. However, there was no information on how anesthetic affects local and systemic cellular immune function. We conducted this study to examine the impact of dex on the differentiation and function of immune cells at site of inflammation and in peripheral blood during endotoxemia of mice. In BALB/c mice with and without endotoxemia, we evaluated the influence of two dosages of 5 and 50 mcg/kg/h intravenous dex on immune cells: including number of T cells (CD3), B cells (CD19), natural killer cells (CD8a), monocytes (CD11b), and macrophages (Mac‐3) in peripheral blood, the activities of macrophages in peripheral blood and in peritoneal lavage, and proliferation of B and T cells and of natural killer cells activity in the spleen. Endotoxemia increased the number of CD3 T cells, CD 19 B cells and macrophages in the peripheral blood, augmented macrophage activity in the peritoneum, and increased T cell proliferation and natural killer cell activity in the spleen. Further administration of 5 mcg/kg/h dex attenuated systemic increase in number of T cells, B cells, and macrophages during endotoxemia and 50 mcg/kg/h dex significantly attenuated the increase in activity of macrophages in the peripheral blood during endotoxemia. In the peritoneum, however, 5 mcg/kg/h dex preserved and 50 mcg/kg/h dexmedetomidine enhanced the activity of macrophages during endotoxemia. Increased in proliferation of T cells in spleen during endotoxemia was attenuated by both doses of dex. Last, 50 mcg/kg/h dex enhanced natural killer cells activity during endotoxemia. While preserving the effects of endotoxemia on macrophage's activity in the infection site and natural killer cell's activity in the spleen, dex decreased systemic fulminant immune reaction in endotoxemia, by attenuating the augmented response in the number of T cells, B cells and macrophages, activity of macrophages in the peripheral blood, and proliferation of T cells in spleen during endotoxemia. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1416–1422, 2015.
Keywords:dexmedetomidine  endotoxemia  BALB/c mice  immunomodulation
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