重症难治性休克发生机制的若干进展

Advances in the pathogenesis of shock

重症难治性休克是当前休克研究的主攻目标之一。线粒体功能紊乱参与了休克和多器官功能不全的发生。治疗后毛细血管无复流现象使功能性毛细血管密度(FCD)下降,是预后不良的征象。治疗后顽固性低血压导致重要生命器官灌流不足,也是引起死亡的重要原因。过量输液治疗导致的血液重度稀释和低黏血症也使FCD下降,影响了抢救存活率。本文就上述问题的发生机制进行了阐述。

Irreversible shock is one of the major target in shock research. The dysfunction of mitochondria involves in the pathogenesis of shock and MODS. Capillary no-reflow post-treatment leads to decrease of functional capillary density (FCD), which is a predictor of bad prognosis. Refractory hypotension after treatment results in low perfusion of vital organ, which is also one of the causes for death. Hypovisosaemia is a problem in shock treatment with massive fluid infusion leading to the decrease of FCD and survival rate. The mechanisms of the issues mentioned above are discussed in the text.