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

机译:Dexmedetomidine在产后出血诱导的大鼠中的多器官功能障碍综合征期间降低细胞因子释放

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摘要

Dexmedetomidine (DEX) is an a2-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.
机译:右丁咪啶(Dex)是A2-肾上腺素能激动剂。 它降低了去甲肾上腺素释放的水平,导致突触后的肾上腺素能活性减少。 在本研究中,在大鼠中研究了DEX对产后出血诱导的多器官功能障碍综合征(BMODS)的影响,其中通过低血压和夹层动脉的夹紧组合诱导BMOD。 我们在大鼠产后BMODS期间评估了右甲酰嘌呤胺(DEX)在细胞因子释放中的作用。 总之,本研究表明,在产后BMOD期间,DEX给药减少了IFN-R和IL-4释放和降低肺损伤。 通过抑制炎症和自由基释放独立于DEX剂量,可以通过抑制炎症和自由基释放来降低BMOD中的炎症细胞因子产生。

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