中文摘要：

背景脓毒症是机体对感染的反应失调而导致危及生命的多器官功能障碍。虽然目前针对脓毒症有一些治疗措施，但脓毒症和脓毒症休克仍是导致危重症患者死亡的首要原因。心肌损伤是脓毒症的常见并发症，会导致左室和右室泵功能衰竭。参与脓毒症心肌损伤的物质和机制很多，包括毒紊、细胞因子、一氧化氮、补体激活、凋亡和能量代谢紊乱等。然而，关于脓毒症心肌损伤的潜在分子机制尚未完全清楚。目的讨论可能导致脓毒症心肌损伤线粒体功能异常的机制。内容关于脓毒症心肌损伤研究比较多的是线粒体功能异常，目前研究认为线粒体功能损伤涉及许多机制，导致线粒体能量耗竭，最终导致心肌损伤。而对于线粒体功能的损伤和修复机制仍存在争议。趋向关于脓毒症的研究不断升温，新的研究工具的出现为将来有效的特异性治疗方法的出现奠定了基础。

英文摘要：

Background Sepsis is the abnormal immune and inflammatory response to infection that may ultimately result in multi-organ failure. Lacking of effective therapy, sepsis and septic shock remain as leading causes of death, especially in patients that sepsis led to severe myocardial dysfunction. However, the mechanisms underlying myocardial injury following sepsis are not clear. Objective This review discusses that sepsis may cause cardiomyopathy through damaging mitochondrial function. Content The major manifestations of septic cardiomyopathy include right and left ventricular pump failure. In sepsis, many substances, including toxins, cytokines, reactive oxygen species, and nitric oxide, are released, and subsequently mobilize a series of pathological procedures, such as, calcium overload, mitochondrial dysfunction, autophage, and apoptosis. Mitochondrial dysfunction and energy depletion likely contribute to septic cardiomyopathy. Trend Early diagnosis of myocardial dysfunction and restoration of normal mitochondrial function may be an effective strategy in the treatment of sepsis and septic shock.