Pinsky Michael R
Department of Critical Care Medicine, Bioengineering and Anesthesiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Contrib Nephrol. 2007;156:47-63. doi: 10.1159/000102070.
BACKGROUND/AIMS: Sepsis and multiple organ failure are complex processes that result from dysregulation of the immune response and its associated hematological, hemodynamic and metabolic disturbances.
Review of the pathophysiological basis for sepsis and a review of the literature on its mechanisms of expression.
Sepsis is the host response to an injury, often infectious in origin, that creates both pro- and anti-inflammatory immune responses. The level and duration of this response roughly correlates with outcome. Subcellular injury characterized by increased oxidative stress defines the central mitochondrial component of this process. Treatments which minimize the amplification of this response are usually more effective at reducing tissue injury than are measures aimed at suppressing the inflammatory response.
Sepsis is a complex process whose expression and treatment are just now being defined. Treatments that minimize the overall host response still represent the most effective strategies.
背景/目的：脓毒症和多器官功能衰竭是复杂的过程，由免疫反应失调及其相关的血液学、血流动力学和代谢紊乱引起。
回顾脓毒症的病理生理基础，并综述其表达机制的相关文献。
脓毒症是宿主对损伤（通常源于感染）的反应，会产生促炎和抗炎免疫反应。这种反应的程度和持续时间大致与预后相关。以氧化应激增加为特征的亚细胞损伤定义了该过程的核心线粒体成分。与旨在抑制炎症反应的措施相比，将这种反应的放大降至最低的治疗方法通常在减少组织损伤方面更有效。
脓毒症是一个复杂的过程，其表达和治疗目前正在被明确。将整体宿主反应降至最低的治疗方法仍然是最有效的策略。
