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细胞病变性缺氧。一种解释脓毒症中器官功能障碍的概念。

Cytopathic hypoxia. A concept to explain organ dysfunction in sepsis.

作者信息

Fink M P

机构信息

Critical Care Medicine, Division University of Pittsburgh Medical School, USA.

出版信息

Minerva Anestesiol. 2000 May;66(5):337-42.

Abstract

The most common cause of death in patients with sepsis is the multiple organ dysfunction syndrome (MODS). One important factor underlying the pathogenesis of MODS may be sepsis-induced alterations in cellular energy metabolism due to acquired intrinsic derangements in cellular respiration, a phenomenon that might be called "cytopathic hypoxia". A number of different biochemical mechanisms have been postulated to account for cytopathic hypoxia in sepsis, including reversible inhibition of cytochrome oxidase by nitric oxide, irreversible inhibition of one or more mitochondrial respiratory complexes by peroxynitrite, and activation of the nuclear enzyme, poly-(ADP-ribosyl)-polymerase.

摘要

脓毒症患者最常见的死亡原因是多器官功能障碍综合征(MODS)。MODS发病机制的一个重要因素可能是由于细胞呼吸获得性内在紊乱导致脓毒症引起的细胞能量代谢改变,这种现象可称为“细胞病性缺氧”。为解释脓毒症中的细胞病性缺氧,人们提出了许多不同的生化机制,包括一氧化氮对细胞色素氧化酶的可逆性抑制、过氧亚硝酸盐对一种或多种线粒体呼吸复合物的不可逆性抑制,以及核酶聚(ADP - 核糖基)聚合酶的激活。

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