Mitochondrial Dysfunction and Resuscitation in Sepsis

被引：63

作者：

Ruggieri, Albert J. ^{[1
,3
]}

Levy, Richard J. ^{[2
,3
]}

Deutschman, Clifford S. ^{[1
,3
]}

机构：

[1] Univ Penn, Sch Med, Dept Anesthesiol & Crit Care, Philadelphia, PA 19104 USA

[2] Childrens Natl Med Ctr, Div Anesthesiol & Pain Med, Washington, DC 20010 USA

[3] Univ Penn, Sch Med, Stavropoulos Sepsis Res Program, Philadelphia, PA 19104 USA

来源：

CRITICAL CARE CLINICS | 2010年 / 26卷 / 03期

关键词：

Sepsis; Mitochondria; Mitochondrial dysfunction; Cytopathic hypoxia; Electron transport; Cytochrome c; ATP; CYTOCHROME-OXIDASE ACTIVITY; CYTOPATHIC HYPOXIA; NITRIC-OXIDE; INHIBITION; RESTORES; METABOLISM;

D O I：

10.1016/j.ccc.2010.04.007

中图分类号：

R4 [临床医学];

学科分类号：

100218 [急诊医学];

摘要：

Sepsis is among the most common causes of death in patients in intensive care units in North America and Europe. In the United States, it accounts for upwards of 250,000 deaths each year. Investigations into the pathobiology of sepsis have most recently focused on common cellular and subcellular processes. One possibility would be a defect in the production of energy, which translates to an abnormality in the production of adenosine triphosphate and therefore in the function of mitochondria. This article presents a clear role for mitochondrial dysfunction in the pathogenesis and pathophysiology of sepsis. What is less clear is the teleology underlying this response. Prolonged mitochondrial dysfunction and impaired biogenesis clearly are detrimental. However, early inhibition of mitochondrial function may be adaptive.

引用

页码：567 / +

页数：11

共 34 条

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