线粒体功能不全在重症休克发生中的作用

Role of mitochondrial dysfunction in genesis of severe shock

重症休克是指休克的晚期,在输血补液及其它抗休克治疗以后,病人生命仍难以抢救。它是世界范围内致死、致残的主要疾患之一。已证明休克时小动脉平滑肌细胞（arteriolar smooth muscle cells,ASMCs）ATP含量减少,引起ATP敏感钾通道（KATP）开放和ASMCs超极化,是导致重症休克血管反应性下降和顽固性低血压的重要原因。

The high mortality is a leading element of human health that follows severe shock even after blood transfusion and other anti - shock therapy. Therefore, to find out the mechanism of high mortality in severe shock is very critical. As a hotspot in recent years, mitochondrial function has important value in the genesis of many diseases, such as cardiovascular diseases, diabetes mellitus, Alzheimer disease, Parkinsen disease, nonalcoholic steatohepatitis and so on. Mitochondrial dysfunction often takes place in relation to the opening of mitochondrial permeability transition pore with in- tracellular low ATP content in severe shock. The consequence of intraceUular low ATP content may lead to the dysfunction of various organs with difficult treatment of severe shock. Therefore, protection against mitochondrial damage is a novel ap- preach for treatment of Severe shock. This article summarizes the concept, pathogenesis, detection variables and treatment of mitochondrial dysfunction in severe shock.