脓毒血症致急性肾损伤及右美托咪定保护作用机制研究进展

发布时间：2018-06-13 08:17

本文选题：SAKI + 发病机制　；参考：《东北农业大学学报》2017年06期

【摘要】：脓毒血症可造成机体多器官、组织继发性损伤,其中肾脏是最易受其侵害脏器之一。脓毒血症致急性肾损伤(Septic acute kidney injury,SAKI)是病患预后不良、高死亡率主要原因,但SAKI发病机制、治疗药物作用靶位以及保护作用尚不明确。以往认为SAKI主要由肾脏血流动力学改变导致肾小管上皮细胞坏死造成,近年研究发现,血流动力学改变并非其最主要病理生理机制,还包括由内毒素介导的炎症反应、肾脏细胞凋亡、凝血功能异常致肾小球内栓塞以及坏死细胞造成肾小管阻塞等。右美托咪定(Dexmedetomidine,DEX)对SAKI具一定保护作用,其保护机制尚无定论,多集中在抑制肾脏炎性因子产生,减轻氧化应激反应及细胞凋亡等方面。DEX具体分子作用机制和药效靶位尚不清楚,有待进一步研究。
[Abstract]:Sepsis can cause multiple organs and secondary injuries in the body, among which the kidney is one of the most vulnerable organs. Acute renal injury caused by sepsis (Septic acute kidney injury, SAKI) is the main cause of poor prognosis and high mortality. However, the pathogenesis of SAKI, the target position of therapeutic drugs and the protective effect are not yet clear. In recent years, studies have found that hemodynamic changes are not the most important pathophysiological mechanisms of renal tubular epithelial cell necrosis caused by renal hemodynamic changes, which include endotoxin mediated inflammatory reactions, renal cell apoptosis, abnormal coagulation function in glomerular embolism and necrotic cells causing renal tubular obstruction. Dexmedetomidine (DEX) has a certain protective effect on SAKI, and its protective mechanism is still not conclusive. It is not clear that the mechanism of the action of.DEX and the target target of the oxidative stress reaction and cell apoptosis are still unclear, and further study is needed.
【作者单位】：东北农业大学动物医学学院;
【基金】：国家重点研发计划(2016YED0501008) 黑龙江省博士后科研启动金项目(LBH-Q14018) 东农学者计划“学术骨干”项目(15XG18) 黑龙江省重点实验室“实验动物与比较医学研究实验中心”专项基金
【分类号】：S854

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