Fink M P
Division of Critical Care Medicine, University of Pittsburgh Medical School, Pittsburgh, Pennsylvania, USA.
Crit Care Clin. 2001 Jan;17(1):219-37. doi: 10.1016/s0749-0704(05)70161-5.
Several lines of evidence support the notion that cellular energetics are deranged in sepsis, not on the basis of inadequate tissue perfusion, but rather on the basis of impaired mitochondrial respiration and/or coupling; that is, organ dysfunction in sepsis may occur on the basis of cytopathic hypoxia. If this concept is correct, then the therapeutic implications are enormous. Efforts to improve outcome in patients with sepsis by monitoring and manipulating cardiac output, systemic Do2, and regional blood flow are doomed to failure. Instead, the focus should be on developing pharmacologic strategies to restore normal mitochondrial function and cellular energetics.
多条证据支持这样一种观点，即脓毒症时细胞能量代谢紊乱，其并非基于组织灌注不足，而是基于线粒体呼吸和/或耦联受损；也就是说，脓毒症时的器官功能障碍可能基于细胞病性缺氧而发生。如果这一概念正确，那么其治疗意义将是巨大的。通过监测和调控心输出量、全身氧输送（Do2）和局部血流来改善脓毒症患者预后的努力注定会失败。相反，重点应放在开发恢复线粒体正常功能和细胞能量代谢的药理学策略上。
