蒋晓芳　宋云林　程玺　王于强　通耀威

[关键词] 脓毒症;心肌抑制;脓毒性心肌病模型;左西孟旦

[中图分类号] R43          [文献标识码] A          [文章编号] 1673-9701（2021）18-0188-05

Research progress of levosimendan on animal model of septic cardiomyopathy

JIANG Xiaofang1   SONG Yunlin2   CHENG Xi1   WANG Yuqiang1   TONG Yaowei1

1.Xinjiang Medical University， Urumqi   830011， China; 2.Intensive Care Unit，The First Affiliated Hospital of Xinjiang Medical University，Urumqi   830011，China

[Abstract] Sepsis is the maladjustment of the host response to infection，which leads to life-threatening organ dysfunction. Sepsis often occurs on the basis of clinical acute and critical diseases such as burns，infections and multiple injuries，and it is also one of the important reasons leading to multiple organ dysfunction syndrome （MODS）[2]. Sepsis-induced myocardial dysfunction （SIMD） is one of the common complications of severe sepsis and septic shock [3].It is an important factor leading to multiple organ dysfunction and increased mortality in sepsis.Levosimendan is the first calcium sensitizer approved for the treatment of severe cardiac failure，which has been widely used in the treatment of patients with coronary heart disease and cardiac failure and has also been used in sepsis. Animal experiments show that levosimendan can improve cardiac function，reduce peripheral vascular resistance，dilate pulmonary artery and improve gastrointestinal function in septic animals. Because the decrease of myofilament calcium sensitivity has been repeatedly confirmed in experimental septic cardiomyopathy，it is speculated that calcium sensitizers may also improve myocardial dysfunction caused by sepsis.However，the role of calcium sensitizer in septic cardiomyopathy has not been thoroughly researched. Therefore，the research progress of levosimendan on cardiac function mechanism of septic cardiomyopathy animal model was reviewed in this paper.

[Key words] Sepsis;Myocardial inhibition;Septic cardiomyopathy model;Levosimendan

脓毒症被定义为感染引起的宿主反应失调导致的危及生命的器官功能障碍[1-8]，脓毒性休克是脓毒症时全身循环和代谢异常出现的最严重情况，具有高病死率。19世纪60年代，人们已经发现脓毒症早期就可出现心肌的损伤，大量研究表明，在脓毒性休克期间存在心肌损伤及心肌抑制，表现为左、右心室射血分数（LVEF/RVEF）下降及舒张功能减退，脓毒性休克合并心脏功能损伤后病死率会明显增加[9]。流行病学调查显示，脓毒症患者中有40%并发心肌损伤，而入住ICU的脓毒症休克患者中约有60%具有心肌损伤的临床表现，并且脓毒症心肌损伤的患者死亡率可达70%～90%[10]。心脏仅是心血管系统中的一部分，但它要不断适应外周血流动力学的变化，因此，很难区分，是脓毒症直接导致心肌损伤，或在脓毒症中心脏不断适应前负荷、后负荷以及神经体液活动等的变化而间接导致心肌损伤。只有深入了解脓毒症心肌抑制的发病机制，才可能精确地进行临床治疗，从而降低脓毒症心肌抑制的发病率和死亡率。目前脓毒症心肌损伤的机制大多考虑可能与血流动力学异常、基因、分子、代谢以及心肌自身结構改变有关[11]，针对脓毒症心肌损伤的治疗方面，除了适当管理感染外，关注血流动力学稳定是脓毒性心肌病患者的首要步骤，建议通过监测液体反应参数指导快速有效的液体治疗，以纠正血容量不足，作为脓毒症治疗的基石[12]。……