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脓毒症中的氧化应激和线粒体功能障碍。

Oxidative stress and mitochondrial dysfunction in sepsis.

机构信息

Academic Unit of Anaesthesia and Intensive Care, School of Medicine and Dentistry, University of Aberdeen, Aberdeen, UK.

出版信息

Br J Anaesth. 2011 Jul;107(1):57-64. doi: 10.1093/bja/aer093. Epub 2011 May 19.

Abstract

Sepsis-related organ dysfunction remains the most common cause of death in the intensive care unit (ICU), despite advances in healthcare and science. Marked oxidative stress as a result of the inflammatory responses inherent with sepsis initiates changes in mitochondrial function which may result in organ damage. Normally, a complex system of interacting antioxidant defences is able to combat oxidative stress and prevents damage to mitochondria. Despite the accepted role that oxidative stress-mediated injury plays in the development of organ failure, there is still little conclusive evidence of any beneficial effect of systemic antioxidant supplementation in patients with sepsis and organ dysfunction. It has been suggested, however, that antioxidant therapy delivered specifically to mitochondria may be useful.

摘要

尽管医疗保健和科学取得了进步,但与脓毒症相关的器官功能障碍仍然是重症监护病房(ICU)中最常见的死亡原因。脓毒症固有炎症反应导致的明显氧化应激会引发线粒体功能变化,从而导致器官损伤。通常,一个相互作用的抗氧化防御复杂系统能够抵抗氧化应激,防止线粒体损伤。尽管氧化应激介导的损伤在器官衰竭的发展中起着公认的作用,但在脓毒症和器官功能障碍患者中,系统抗氧化剂补充的任何有益效果仍缺乏确凿证据。然而,有人认为,专门递送到线粒体的抗氧化治疗可能是有用的。

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