线粒体功能障碍与败血症休克的严重程度和结果之间的关联
David Brealey1, Michael Brand, Iain Hargreaves
1Bloomsbury Institute of Intensive Care Medicine, Wolfson Institute of Biomedical Research and Department of Medicine, University College London, London W1T 3AA, UK.
Lancet (London, England)
|July 23, 2002
概括
败血症导致线粒体功能障碍和ATP水平低,与器官衰竭和不良结果有关. 氧化的过度生产和抗氧化剂的枯竭导致了重症患者的这种生物能量失效.
科学领域:
- 临界护理医学 临界护理医学
- 生物化学 生物化学
- 病理生理学 病理生理学
背景情况:
- 败血症引起的多器官衰竭是重症患者死亡的主要原因.
- 败血症中器官功能障碍的机制尚未完全理解.
- 败血症中组织氧气水平升高表明氧气利用受损,可能是由于线粒体功能障碍.
研究的目的:
- 调查线粒体功能障碍在败血症引起的器官衰竭中的作用.
- 探索氧化物生产,抗氧化剂状态和败血症患者的线粒体功能之间的关联.
主要方法:
- 骨肌肉活检对28名重症败血症患者和9名健康对照进行.
- 分析包括呼吸链酶活性 (复合物I-IV),ATP度,降低的谷氨和酸盐/酸盐水平.
主要成果:
- 死亡的败血症患者的骨肌ATP度明显低于幸存者和对照人群.
- 复合I活性与冲击严重程度和氧化标志物相反相关,与降低的谷氨和ATP水平相对正相关.
结论:
- 在败血症患者中,氧化过量产生,抗氧化剂耗尽,线粒体功能障碍和ATP减少之间存在关联.
- 这些因素与器官衰竭和患者的结果相关.
- 生物能衰竭被认为是败血症引起的多器官功能障碍的一个关键机制.
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