Bloomsbury Institute of Intensive Care Medicine, Division of Medicine, University College London, Cruciform Building, Gower St, WC1E 6BT London, UK.
UCL Consortium for Mitochondrial Research, Department of Cell and Developmental Biology, University College London, Medical Sciences Building, Gower St, WC1E 6BT London, UK.
Biochim Biophys Acta Mol Basis Dis. 2019 Apr 1;1865(4):759-773. doi: 10.1016/j.bbadis.2018.10.011. Epub 2018 Oct 17.
Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Myocardial dysfunction, often termed sepsis-induced cardiomyopathy, is a frequent complication and is associated with worse outcomes. Numerous mechanisms contribute to sepsis-induced cardiomyopathy and a growing body of evidence suggests that bioenergetic and metabolic derangements play a central role in its development; however, there are significant discrepancies in the literature, perhaps reflecting variability in the experimental models employed or in the host response to sepsis. The condition is characterised by lack of significant cell death, normal tissue oxygen levels and, in survivors, reversibility of organ dysfunction. The functional changes observed in cardiac tissue may represent an adaptive response to prolonged stress that limits cell death, improving the potential for recovery. In this review, we describe our current understanding of the pathophysiology underlying myocardial dysfunction in sepsis, with a focus on disrupted mitochondrial processes.
脓毒症定义为一种危及生命的器官功能障碍，由宿主对感染的失调反应引起。心肌功能障碍，通常称为脓毒症性心肌病，是一种常见的并发症，并与更差的预后相关。许多机制导致脓毒症性心肌病，越来越多的证据表明，生物能量和代谢紊乱在其发展中起着核心作用；然而，文献中存在显著差异，这可能反映了所采用的实验模型或宿主对脓毒症的反应的变异性。该病症的特征是缺乏明显的细胞死亡、正常的组织氧水平，并且在幸存者中，器官功能障碍是可逆的。在心脏组织中观察到的功能变化可能代表对延长的应激的适应性反应，限制了细胞死亡，提高了恢复的潜力。在这篇综述中，我们描述了我们对脓毒症中心肌功能障碍的病理生理学的现有理解，重点是线粒体过程的破坏。
